Publications by authors named "Yingqi Zhu"

29 Publications

  • Page 1 of 1

Optimal dose of physical exercise for preventing cardiac and renal dysfunction, data from NHANES survey.

Eur J Prev Cardiol 2022 May 17. Epub 2022 May 17.

Department of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Shock and Microcirculation, National Clinical Research Center of Kidney Disease, Guangdong Provincial Institute of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1093/eurjpc/zwac096DOI Listing
May 2022

miR-142-3p suppresses porcine reproductive and respiratory syndrome virus (PRRSV) infection by directly targeting Rac1.

Vet Microbiol 2022 Jun 14;269:109434. Epub 2022 Apr 14.

State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University, Beijing 100193, China; Ministry of Agriculture Key Laboratory of Soil Microbiology, College of Biological Sciences, China Agricultural University, Beijing 100193, China; Department of Microbiology and Immunology, College of Biological Sciences, China Agricultural University, Beijing 100193, China. Electronic address:

Porcine reproductive and respiratory syndrome (PRRS) caused by PRRS virus (PRRSV) has been recognized as one of the severest epidemics in pigs worldwide. microRNAs (miRNAs) play important roles in a variety of biological processes, including cell differentiation, proliferation and death, as well as viral infections and antiviral immune responses. In this study, we found that miR-142-3p was expressed lower in cells susceptible to PRRSV infection than in cells less or no permissive to PRRSV infection. Subsequently, we showed that overexpression of miR-142-3p remarkably inhibited PRRSV infection in PAMs, while blockage of endogenous miR-142-3p significantly enhanced PRRSV replication. Then, we demonstrated that miR-142-3p directly targeted Ras-related C3 botulinum toxin substrate 1 (Rac1), a member of Rho GTPases family, by using luciferase reporter assay and UV cross-linking and immunoprecipitation (CLIP) assay. Importantly, we verified that miR-142-3p inhibited PRRSV entry into PAMs and accordingly suppressed PRRSV infection by downregulating Rac1 expression. These findings reveal an important role of miR-142-3p in modulating PRRSV infection and provide us with some ideas for developing novel antiviral therapy against PRRSV infection.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.vetmic.2022.109434DOI Listing
June 2022

Autophagy and Exosome Coordinately Enhance Macrophage M1 Polarization and Recruitment in Influenza A Virus Infection.

Front Immunol 2022 17;13:722053. Epub 2022 Mar 17.

Department of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.

Background: Influenza A virus infection results in viral pneumonia, which is often accompanied by the infiltration and recruitment of macrophages, overactivation of inflammatory responses, and obvious cell autophagy and exosome production. However, little is known about the roles of autophagy and exosome production in these inflammatory responses.

Methods: In this study, multiple methods, such as flow cytometry, real-time quantitative reverse transcription-polymerase chain reaction, immune-fluorescence technology, and western blot, were applied to explore the possible effects of autophagy and exosome production by H1N1-infected host cells.

Results: It was observed that a high number of polarized macrophages (CD11b/F4/80/CD86) were recruited to the lung tissues of infected mice, which could be mimicked by tracking the movement of macrophages to H1N1-infected cells (transwell assays). Furthermore, there was some coordinated upregulation of M1 polarization signs (iNOS/Arg-1 bias) as well as autophagy (LC3) and exosome (CD63) biomarkers in the infected macrophages and epithelial cells. Moreover, exosomes extracted from the supernatant of virus-infected cells were shown to promote the recruitment and polarization of more peritoneal macrophages than the normal group. The fluorescence colocalization of LC3-CD63 and the inhibition of autophagy and exosome signaling pathway further revealed that H1N1 infection seemed to sequentially activate the M1 polarization and recruitment of macrophages autophagy-exosome dependent pathway.

Conclusion: Autophagy and exosome production coordinately enhance the M1 polarization and recruitment of macrophages in influenza virus infection, which also provides potential therapeutic targets.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fimmu.2022.722053DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8967985PMC
April 2022

CX3CL1 Worsens Cardiorenal Dysfunction and Serves as a Therapeutic Target of Canagliflozin for Cardiorenal Syndrome.

Front Pharmacol 2022 18;13:848310. Epub 2022 Mar 18.

Department of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China.

The prognosis of cardiorenal dysfunction induced by diabetes mellitus (DM), which belongs to cardiorenal syndrome type 5, is poor and its pathogenesis remains elusive. We have reported that CX3CL1 exacerbated heart failure and direct inhibition of CX3CL1 improved cardiac function. Emerging evidence supports that CX3CL1 is involved in renal impairment. Here we attempt to clarify whether CX3CL1 might be a therapeutic target for cardiorenal dysfunction in diabetes. We found that cardiac and renal CX3CL1 protein levels were significantly increased in both streptozotocin-induced diabetic mice and in non-obese diabetic mice, and that hyperglycemia led to persistent CX3CL1 expression in the heart and kidneys even after it was controlled by insulin. In cultured cardiac and renal cells, soluble CX3CL1 accelerated mitochondrial-dependent apoptosis via activation of the RhoA/ROCK1-Bax signaling pathway and promoted fibrosis through cellular phenotypic trans-differentiation mediated by the TGF-β/Smad pathway. In the two diabetic mouse models, knockout of CX3CL1 receptor CX3CR1 or treatment with an CX3CL1 neutralizing antibody significantly improved cardiorenal dysfunction by inhibiting apoptosis, mitochondrial dysfunction, and fibrosis. Moreover, sodium glucose cotransporter 2 inhibitor canagliflozin significantly downregulated cardiac and renal CX3CL1 expression and improved cardiorenal dysfunction. These findings indicate that CX3CL1 could be a new therapeutic target for diabetes-induced cardiorenal dysfunction.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fphar.2022.848310DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8971671PMC
March 2022

Development of a potential diagnostic monoclonal antibody against capsid spike protein VP27 of the novel goose astrovirus.

Poult Sci 2022 Mar 23;101(3):101680. Epub 2021 Dec 23.

College of Animal Science and Technology, Anhui Agricultural University, Hefei 230036, China; Anhui Province Key Laboratory of Veterinary Pathobiology and Disease Control, Hefei 230036, China. Electronic address:

Goose astrovirus (GAstVs) is an emerging pathogen of goslings that causes fatal gout, kidney hemorrhages, renomegaly, and high mortality. The GAstVs VP27 protein is an important capsid protein and a candidate for the development of diagnostic reagents. The aim of this study was to clone and express the VP27 gene for preparation of a specific monoclonal antibody (mAb). The VP27 protein was expressed and purified in the supernatant of Escherichia coli BL21. Then, the mAb was obtained with the hybridoma technique and named 2AF11. It was differentiated as IgG1 with the help of immunoglobulin subclass tests. This mAb can specifically recognize the VP27 protein in GAstVs-infected cells, as evidenced by western blot analysis and immunofluorescent assay. Furthermore, this mAb could also detect the VP27 protein in GAstVs-infected tissues, as demonstrated by immunohistochemistry. These findings indicate that this mAb has high diagnostic potential. Therefore, the newly produced anti-VP27 mAb, 2AF11, could be a useful tool as a specific diagnostic marker for GAstVs.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.psj.2021.101680DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8883067PMC
March 2022

A Bibliometric and Visualized Analysis of Cardiac Regeneration Over a 20-Year Period.

Front Cardiovasc Med 2021 13;8:789503. Epub 2021 Dec 13.

State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Shock and Microcirculation, Department of Cardiology, National Clinical Research Center of Kidney Disease, Guangdong Provincial Institute of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Recent research has suggested that cardiac regeneration may have the widely applicable potential of treating heart failure (HF). A comprehensive understanding of the development status of this field is conducive to its development. However, no bibliometric analysis has summarized this field properly. We aimed to analyze cardiac regeneration-related literature over 20 years and provide valuable insights. Publications were collected from the Web of Science Core Collection (WoSCC). Microsoft Excel, VOSviewer, CiteSpace, and alluvial generator were used to analyze and present the data. The collected 11,700 publications showed an annually increasing trend. The United States and Harvard University were the leading force among all the countries and institutions. The majority of articles were published in Circulation Research, and Circulation was the most co-cited journal. According to co-citation analysis, burst detection and alluvial flow map, cardiomyocyte proliferation, stem cells, such as first-and second-generation, extracellular vesicles especially exosomes, direct cardiac reprogramming, macrophages, microRNAs, and inflammation have become more and more popular recently. Cardiac regeneration remains a research hotspot and develops rapidly. How to modify cardiac regeneration endogenously and exogenously may still be the hotspot in the future and should be discussed more deeply.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fcvm.2021.789503DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8710530PMC
December 2021

Targeting Wnt Signaling in the Tumor Immune Microenvironment to Enhancing EpCAM CAR T-Cell therapy.

Front Pharmacol 2021 1;12:724306. Epub 2021 Nov 1.

Shanghai Engineering Research Center of ImmunoTherapeutics, Fudan University, Shanghai, China.

Colorectal cancer (CRC) patients are still lacking viable treatments. Chimeric antigen receptor (CAR) T cells have shown promise in hematologic malignancies, but their efficacy in solid tumors has been limited due to the immunosuppressive tumor microenvironment. We found that cancer antigen- EpCAM expression increased in the metastatic stage compared with the primary stage in cancers and the activation of Wnt and TGFβ pathways was positively correlated with EpCAM expression in multiple cancers, including colorectal cancer. We constructed CAR T cells targeting EpCAM that successfully showed selective cytotoxicity in highly EpCAM-expressing cancer cell lines. The combination of EpCAM CAR-T with the Wnt inhibitor-hsBCL9-24 displayed synergetic effect against EpCAM-positive colon cells and also . A mechanistic study showed that hsBCL9-24 treatment could modulate the tumor environment and improve infiltration of T cells, while possibly promoting the effector T cells at the early stages and postponing the exhaustion of CAR T cells at advanced stages. Overall, these results demonstrated that the combination of EpCAM CAR T-cell therapy with the Wnt inhibitor can overcome the limitations of CAR T cells in treating solid tumors.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fphar.2021.724306DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8591126PMC
November 2021

Phencynonate hydrochloride exerts antidepressant effects by regulating the dendritic spine density and altering glutamate receptor expression.

Behav Pharmacol 2021 12;32(8):660-672

Institute of Brain and Behavioural Sciences, College of Life Science, Shaanxi Normal University, Xi'an, Shaanxi.

Phencynonate hydrochloride (PCH) is a drug that crosses the blood-brain barrier. Cellular experiments confirmed that PCH protects against glutamate toxicity and causes only weak central inhibition and limited side effects. As shown in our previous studies, PCH alleviates depression-like behaviours induced by chronic unpredictable mild stress (CUMS). Here we administered PCH at three different doses (4, 8 and 16 mg/kg) to male rats for two continuous days after CUMS and conducted behavioural tests to assess the dose-dependent antidepressant effects of PCH and its effects on the neuroplasticity in the hippocampus and medial prefrontal cortex (mPFC). Meanwhile, we measured the spine density and expression of related proteins to illustrate the mechanism of PCH. PCH treatment (8 mg/kg) significantly alleviated depression-like behaviours induced by CUMS. All doses of PCH treatment reversed the spine loss in prelimbic and CA3 regions induced by CUMS. Kalirin-7 expression was decreased in the hippocampus and mPFC of the CUMS group. The expression of the NR1 and NR2B subunits in the hippocampus, and NR2B in mPFC are increased by CUMS. PCH treatment (8 and 16 mg/kg) reversed all of these changes of Kalirin-7 in PFC and hippocampus, as well as NR1 and NR2B expression in the hippocampus. PCH is expected to be developed as a new type of rapid antidepressant. Its antidepressant effect may be closely related to the modulation of dendritic spine density in the prelimbic and CA3 regions and the regulation of Kalilin-7 and N-methyl-D-aspartic acid receptor levels in the hippocampus.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1097/FBP.0000000000000660DOI Listing
December 2021

Antiviral and virucidal activities of lycorine on duck tembusu virus in vitro by blocking viral internalization and entry.

Poult Sci 2021 Oct 25;100(10):101404. Epub 2021 Jul 25.

College of Animal Science and Technology, Anhui Agricultural University, Hefei 230036, China; Anhui Province Key Laboratory of Veterinary Pathobiology and Disease Control, Hefei 230036, China. Electronic address:

Duck tembusu virus (DTMUV) was firstly identified in 2010 in China; since then, it has caused enormous economic loss to breeding industry. Great efforts have been made to develop drugs and vaccines against DTMUV. However, current available vaccines or anti-DTMUV drugs are consistently inefficient. Hence, various more broadly effective drugs have become important for the treatment of DTMUV infection; among these, lycorine, one of the important sources of active alkaloids, is a promising example. Nevertheless, it is not known whether lycorine has any antiviral activities against DTMUV. Therefore, the purpose of the present study is to investigate the anti-DTMUV abilities of lycorine. The cytotoxicity of lycorine was evaluated on BHK-21 cells by CCK-8 assay, and its antiviral effect against DTMUV was examined by real-time PCR assays, virus titer determination, Western blot and immunofluorescence (IFA) assays, respectively. Furthermore, the underlying mechanisms of the anti-DTMUV effects of lycorine were also investigated. The results indicated that the highest nontoxicity concentration of lycorine on BHK-21 cells was 5 µM. Lycorine possessed the antiviral ability against DTMUV on BHK-21 cells, as demonstrated by the reduction of virus titers and copy numbers in vitro. Western blot and IFA analysis showed the inhibitory effect of lycorine on DTMUV envelope (E) protein expression. Moreover, using time-of-addition assays, we found that lycorine displays its antivirus and virucidal activities through blocking viral internalization and entry in vitro. Taken together, our findings firstly demonstrate the antiviral activities of lycorine against DTMUV, suggesting that lycorine can be a potential drug for the treatment of DTMUV infection.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.psj.2021.101404DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8414183PMC
October 2021

Growth differentiation factor 11 attenuates cardiac ischemia reperfusion injury via enhancing mitochondrial biogenesis and telomerase activity.

Cell Death Dis 2021 07 2;12(7):665. Epub 2021 Jul 2.

Department of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.

It has been reported that growth differentiation factor 11 (GDF11) protects against myocardial ischemia/reperfusion (IR) injury, but the underlying mechanisms have not been fully clarified. Considering that GDF11 plays a role in the aging/rejuvenation process and that aging is associated with telomere shortening and cardiac dysfunction, we hypothesized that GDF11 might protect against IR injury by activating telomerase. Human plasma GDF11 levels were significantly lower in acute coronary syndrome patients than in chronic coronary syndrome patients. IR mice with myocardial overexpression GDF11 (oe-GDF11) exhibited a significantly smaller myocardial infarct size, less cardiac remodeling and dysfunction, fewer apoptotic cardiomyocytes, higher telomerase activity, longer telomeres, and higher ATP generation than IR mice treated with an adenovirus carrying a negative control plasmid. Furthermore, mitochondrial biogenesis-related proteins and some antiapoptotic proteins were significantly upregulated by oe-GDF11. These cardioprotective effects of oe-GDF11 were significantly antagonized by BIBR1532, a specific telomerase inhibitor. Similar effects of oe-GDF11 on apoptosis and mitochondrial energy biogenesis were observed in cultured neonatal rat cardiomyocytes, whereas GDF11 silencing elicited the opposite effects to oe-GDF11 in mice. We concluded that telomerase activation by GDF11 contributes to the alleviation of myocardial IR injury through enhancing mitochondrial biogenesis and suppressing cardiomyocyte apoptosis.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/s41419-021-03954-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8253774PMC
July 2021

A novel Tembusu virus isolated from goslings in China form a new subgenotype 2.1.1.

Transbound Emerg Dis 2021 May 16. Epub 2021 May 16.

Anhui Province Key Laboratory of Veterinary Pathobiology and Disease Control, Anhui Agricultural University, Hefei, China.

Since 2010, several duck Tembusu viruses (DTMUVs) have been isolated from infected ducks in China, and these virus strains have undergone extensive variation over the years. Although the infection rate is high, the mortality rate is usually relatively low-~5%-30%; however, since fall 2019, an infectious disease similar to DTMUV infection but with a high mortality rate of ~50% in goslings has been prevalent in Anhui Province, China. The present study identified a new Tembusu virus, designated DTMUV/Goose/China/2019/AQ-19 (AQ-19), that is believed to be responsible for the noticeably high mortality in goslings. To investigate the genetic variation of this strain, its entire genome was sequenced and analysed for specific variations, and goslings and mice were challenged with the isolated virus to investigate its pathogenicity. The AQ-19 genome shared only 94.3%-96.9% and 90.9% nucleotide identity with other Chinese and Malaysian DTMUVs, respectively; however, AQ-19 has high homology with Thailand DTMUVs (97.2%-98.1% nucleotide identity). Phylogenetic analysis of the E gene revealed that AQ-19 and most of Thailand DTMUVs form a branch separate from any of the previously reported DTMUV strains in China. After the challenge, some goslings and mice showed typical clinical signs of DTMUV, particularly severe neurological dysfunction. AQ-19 has high virulence in goslings and mice, resulting in 60% and 70% mortality through intramuscular and intracerebral routes, respectively. Pathological examination revealed severe histological lesions in the brain and liver of the infected goslings and mice. Taken together, these results demonstrated the emergence of a novel Tembusu virus with high virulence circulating in goslings in China for the first time, and our findings highlight the high genetic diversity of DTMUVs in China. Further study of the pathogenicity and host range of this novel Tembusu virus is particularly important.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/tbed.14155DOI Listing
May 2021

Characterizing a long-term chronic heart failure model by transcriptomic alterations and monitoring of cardiac remodeling.

Aging (Albany NY) 2021 04 23;13(10):13585-13614. Epub 2021 Apr 23.

Department of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Lab of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.

The long-term characteristics of transcriptomic alterations and cardiac remodeling in chronic heart failure (CHF) induced by myocardial infarction (MI) in mice are not well elucidated. This study aimed to reveal the dynamic changes in the transcriptome and cardiac remodeling in post-MI mice over a long time period. Monitoring C57BL/6 mice with MI for 8 months showed that approximately 44% of mice died of cardiac rupture in the first 2 weeks and others survived to 8 months with left ventricular (LV) aneurysm. The transcriptomic profiling analysis of cardiac tissues showed that the Integrin and WNT pathways were activated at 8 months after MI while the metabolism-related pathways were inversely inhibited. Subsequent differential analysis at 1 and 8 months post-MI revealed significant enrichments in biological processes, including consistent regulation of metabolism-related pathways. Moreover, echocardiographic monitoring showed a progressive increase in LV dimensions and a decrease in the LV fractional shortening during the first 4 weeks, and these parameters progressed at a lower rate till 8 months. A similar trend was found in the invasive LV hemodynamics, cardiac morphological and histological analyses. These results suggested that mouse MI model is ideal for long-term studies, and transcriptomic findings may provide new CHF therapeutic targets.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.18632/aging.202879DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8202904PMC
April 2021

Highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) induces IL-6 production through TAK-1/JNK/AP-1 and TAK-1/NF-κB signaling pathways.

Vet Microbiol 2021 May 26;256:109061. Epub 2021 Mar 26.

State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University, Beijing, 100193, China; Ministry of Agriculture Key Laboratory of Soil Microbiology, College of Biological Sciences, China Agricultural University, Beijing, 100193, China; Department of Microbiology and Immunology, College of Biological Sciences, China Agricultural University, Beijing, 100193, China. Electronic address:

Porcine reproductive and respiratory syndrome virus (PRRSV) mainly infects monocyte/macrophage lineage and regulates the production of cytokines to influence host immune responses. Interleukin-6 (IL-6) is originally identified as a B-cell stimulatory factor and has important functions in regulating immune response, hemopoiesis, and inflammation. In this study, we verified that highly pathogenic PRRSV (HP-PRRSV) infection up-regulated IL-6 production in vivo and in vitro. Subsequently, we demonstrated that HP-PRRSV infection activated JNK and NF-κB signaling pathways to enhance IL-6 expression. We further showed that TAK-1 was important in the activation of JNK and NF-κB pathways following HP-PRRSV infection. Moreover, AP-1 and NF-κB binding motifs were found in the cloned porcine IL-6 (pIL-6) promoter, and deletion of these motifs abrogated the activation of pIL-6 promoter by HP-PRRSV, suggesting that IL-6 expression is dependent on AP-1 and NF-κB activation. These findings imply that IL-6 induced by HP-PRRSV infection is dependent on the activation of TAK-1/JNK/AP-1 and TAK-1/NF-κB signaling pathways.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.vetmic.2021.109061DOI Listing
May 2021

Antihypertrophic Memory After Regression of Exercise-Induced Physiological Myocardial Hypertrophy Is Mediated by the Long Noncoding RNA Mhrt779.

Circulation 2021 06 24;143(23):2277-2292. Epub 2021 Mar 24.

Department of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Lab of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China (H.L., Y.Z., C.Z., D.H., S.M., L.C., Q.W., Z.C., J.X., Y.Y., X.H., M.K., J.B., Y.L.).

Background: Exercise can induce physiological myocardial hypertrophy (PMH), and former athletes can live 5 to 6 years longer than nonathletic controls, suggesting a benefit after regression of PMH. We previously reported that regression of pathological myocardial hypertrophy has antihypertrophic effects. Accordingly, we hypothesized that antihypertrophic memory exists even after PMH has regressed, increasing myocardial resistance to subsequent pathological hypertrophic stress.

Methods: C57BL/6 mice were submitted to 21 days of swimming training to develop PMH. After termination of exercise, PMH regressed within 1 week. PMH regression mice (exercise hypertrophic preconditioning [EHP] group) and sedentary mice (control group) then underwent transverse aortic constriction or a sham operation for 4 weeks. Cardiac remodeling and function were evaluated with echocardiography, invasive left ventricular hemodynamic measurement, and histological analysis. LncRNA sequencing, chromatin immunoprecipitation assay, and comprehensive identification of RNA-binding proteins by mass spectrometry and Western blot were used to investigate the role of involved in the antihypertrophic effect induced by EHP.

Results: At 1 and 4 weeks after transverse aortic constriction, the EHP group showed less increase in myocardial hypertrophy and lower expression of the and genes than the sedentary group. At 4 weeks after transverse aortic constriction, EHP mice had less pulmonary congestion, smaller left ventricular dimensions and end-diastolic pressure, and a larger left ventricular ejection fraction and maximum pressure change rate than sedentary mice. Quantitative polymerase chain reaction revealed that the long noncoding myosin heavy chain-associated RNA transcript was one of the markedly upregulated lncRNAs in the EHP group. Silencing of attenuated the antihypertrophic effect of EHP in mice with transverse aortic constriction and in cultured cardiomyocytes treated with angiotensin II, and overexpression enhanced the antihypertrophic effect. Using chromatin immunoprecipitation assay and quantitative polymerase chain reaction, we found that EHP increased histone 3 trimethylation (H3K4me3 and H3K36me3) at the a4 promoter of . Comprehensive identification of RNA-binding proteins by mass spectrometry and Western blot showed that can bind SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 (Brg1) to inhibit the activation of the histone deacetylase 2 (Hdac2)/phosphorylated serine/threonine kinase (Akt)/phosphorylated glycogen synthase kinase 3β(p-GSK3β) pathway induced by pressure overload.

Conclusions: Myocardial hypertrophy preconditioning evoked by exercise increases resistance to pathological stress via an antihypertrophic effect mediated by a signal pathway of /Brg1/Hdac2/p-Akt/p-GSK3β.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1161/CIRCULATIONAHA.120.047000DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8177494PMC
June 2021

Epigallocatechin-3-gallate exhibits antiviral effects against the duck Tembusu virus via blocking virus entry and upregulating type I interferons.

Poult Sci 2021 Apr 14;100(4):100989. Epub 2021 Jan 14.

College of Animal Science and Technology, Anhui Agricultural University, Hefei 230036, China; Anhui Province Key Laboratory of Veterinary Pathobiology and Disease Control, Hefei 230036, China. Electronic address:

The duck Tembusu virus (DTMUV) is a novel mosquito-borne Flavivirus which caused huge economic losses for poultry industries in Southeast Asia and China. Currently, no effective antiviral drugs against this virus have been reported. (-)-Epigallocatechin-3-gallate (EGCG), a polyphenol present in abundance in green tea, has recently been demonstrated to have an antiviral activity for many viruses; however, whether EGCG can inhibit DTMUV infection remains unknown. Here, we tried to explore the anti-DTMUV effects and mechanisms of EGCG both in vitro and in vivo. Several EGCG treatment regimens were used to study the comprehensive antiviral activity of EGCG in DTMUV-infected baby hamster kidney cell line (BHK-21). The DTMUV titers of mock- and EGCG-treated infected cell cultures were determined using the tissue culture infective dose assay and the DTMUV mRNA copy number as determined using quantitative Real Time PCR. Moreover, the therapeutic efficacy of EGCG against DTMUV was assessed in DTMUV-infected ducklings. Our results suggested that EGCG significantly reduced the viral infection in BHK-21 cells in a dose-dependent manner, as reflected by the reduction of virus titers, virus copy number, and the expressions of viral E protein. We also observed that EGCG exhibited direct virucidal abilities against DTMUV. Notably, a significant reduction in virus binding ability was also observed, indicating that EGCG possesses excellent inhibitory effects on the viral adsorption step. In addition, DTMUV replication was also suppressed in BHK-21 cells treated with EGCG after viral entry, likely because of upregulation of the levels of interferon alfa and interferon beta. Finally, we also proved that EGCG exhibited anti-DTMUV efficacy in a duckling infection model because the survival rate was significantly improved. This is the first study to demonstrate the protective effect of EGCG against DTMUV, suggesting its potential use as an antiviral drug for DTMUV infection.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.psj.2021.01.012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7921876PMC
April 2021

RNA interactions in right ventricular dysfunction induced type II cardiorenal syndrome.

Aging (Albany NY) 2021 01 20;13(3):4215-4241. Epub 2021 Jan 20.

Department of Cardiology, State Key Laboratory of Organ Failure Research, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.

Right ventricular (RV) dysfunction induced type II cardiorenal syndrome (CRS) has a high mortality rate, but little attention has been paid to this disease, and its unique molecular characteristics remain unclear. This study aims to investigate the transcriptomic expression profile in this disease and identify key RNA pairs that regulate related molecular signaling networks. We established an RV dysfunction-induced type II CRS mouse model by pulmonary artery constriction (PAC). PAC mice developed severe RV hypertrophy and fibrosis; renal atrophy and dysfunction with elevated creatinine were subsequently observed. Expression profiles in RV and kidney tissues were obtained by whole transcriptome sequencing, revealing a total of 741 and 86 differentially expressed (DE) mRNAs, 159 and 29 DEmiRNAs and 233 and 104 DEcircRNAs between RV and kidney tissue, respectively. Competing endogenous RNA (ceRNA) networks were established. A significant alteration in proliferative, fibrotic and metabolic pathways was found based on GO and KEGG analyses, and the network revealed key ceRNA pairs, such as novel_circ_002631/miR-181a-5p/Creb1 and novel_circ_002631/miR-33-y/Kpan6. These findings indicate that significantly dysregulated pathways in RV dysfunction induced type II CRS include Ras, PI3K/Akt, cGMP-PKG pathways, and thyroid metabolic pathways. These ceRNA pairs can be considered potential targets for the treatment of type II CRS.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.18632/aging.202385DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7906202PMC
January 2021

Bibliometric Study of Sodium Glucose Cotransporter 2 Inhibitors in Cardiovascular Research.

Front Pharmacol 2020 15;11:561494. Epub 2020 Sep 15.

Department of Cardiology, State Key Laboratory of Organ Failure Research, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Background: An increasing number of studies have shown that sodium glucose cotransporter 2 (SGLT2) inhibitors, initially used as antidiabetic agents, have cardiovascular (CV) benefits. However, few bibliometric analyses have examined this field systematically. Our study aimed to visualize the publications to determine the trends and hotspots in CV research on SGLT2 inhibitors.

Methods: Publications on SGLT2 inhibitors in cardiovascular research were retrieved from the Web of Science Core Collection. Microsoft Excel 2019, VOSviewer, and CiteSpace V were used to analyze and plot the references.

Results: On July 3, 2020, 1509 records of CV research on SGLT2 inhibitors published from 2013 to 2020 were retrieved. Nearly half were authored by American scholars, and most were published in , , and . The USA was the leading driving force, with a strong academic reputation in this area. Inzucchi SE published the most related articles, while Neal B was cited the most frequently. All the top 10 co-cited references were in the leading co-cited journal, . "Atherosclerotic cardiovascular event" was the leading research hotspot. The keywords "cardiac metabolism," "heart failure hospitalization," and "heart failure with preserved ejection fraction" appeared most recently as research frontiers.

Conclusion: Most studies focused on clinical trial outcomes, such as cardiovascular death and heart failure (HF) hospitalization. The mechanisms of SGLT2 inhibitors, especially those related to cardiac metabolism, may soon become hotspots and should be closely monitored.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fphar.2020.561494DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7522576PMC
September 2020

Coinfection of parvovirus and astrovirus in gout-affected goslings.

Transbound Emerg Dis 2020 Nov 15;67(6):2830-2838. Epub 2020 Jun 15.

Anhui Province Key Laboratory of Veterinary Pathobiology and Disease Control, Anhui Agricultural University, Hefei, China.

Outbreaks of gosling gout have occurred in China since 2017 and caused a considerable economic impact on the poultry industry. While gosling astrovirus (GoAstV) is believed to be the main causal pathogen of gout, the full-blown disease of gout cannot be well reproduced by infecting the goslings with GoAstV, suggesting the possibility of other infectious agents being involved with the development of gosling gout. To assess other possible infectious agents, we collected tissues from gout-affected goslings in 12 goose farms in China, followed by PCR detection of GoAstV, goose reovirus (GRV), goose parvovirus (GPV), fowl adenovirus (FAdV), goose circovirus (GcoV), Tembusu virus (TMUV) and goose haemorrhagic polyomavirus (GHPV). Our data showed that all gout-affected goslings carried both of GoAstV and GPV determined by PCRs, and this was further confirmed by fluorescence multiplex immunohistochemical staining, and phylogenetic analysis of ORF2 gene of GoAstV and VP3 gene of GPV. In addition to the haemorrhage in the kidney, liver, spleen and lung of the gout-affected goslings, histological examinations showed also extensive infiltration of heterophil myelocytes in the kidney, liver, spleen, bursa of Fabricius, thymus, lungs and pancreas. Our findings strongly suggest that coinfection of GoAstV and GPV increases the severity of gout. While this is the first study to report GPV in gout-affected goslings, further studies including infection model are warranted to investigate the role of GPV and its coinfection with GoAstV in the development of gosling gout.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/tbed.13652DOI Listing
November 2020

Overexpression of Na-HCO cotransporter contributes to the exacerbation of cardiac remodeling in mice with myocardial infarction by increasing intracellular calcium overload.

Biochim Biophys Acta Mol Basis Dis 2020 03 26;1866(3):165623. Epub 2019 Nov 26.

Department of Cardiology, State Key Laboratory of Organ Failure Research, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China. Electronic address:

The role of the cardiac isoform of the electrogenic sodium-bicarbonate ion cotransporter (NBCe1) in cardiac remodeling is not fully understood. The aim of this study was to assess the effects of NBCe1 overexpression on cardiac remodeling induced by myocardial infarction (MI) in mice. We generated NBCe1 transgenic (Tg) mice and NBCe1 overexpressing adult mouse ventricular myocytes (AMVMs) to investigate the role of NBCe1 on post-MI remodeling and calcium kinetics. Tg mice showed a markedly higher mortality rate and larger infarct size after MI. At 6 weeks after MI, the maximum rising rates of left ventricular pressure (dp/dt), contractility index, and the exponential time constant of relaxation (τ) were markedly lower, and there was higher cardiomyocyte apoptosis, in Tg mice compared with WT mice. In cultured AMVMs, overexpression of NBCe1 decreased sarcomere shortening and calcium amplitude. In WT AMVMs, the rates of the rise and decay phase of calcium transients, indicated by the rising time (T, time to peak) and decay time constant (τ), and the number of apoptotic cells, were increased following hypoxia, while overexpression of NBCe1 further increased T and cellular apoptosis, but not τ. Intracellular resting calcium and sodium concentrations were significantly increased following both hypoxia and NBCe1 overexpression. Co-treatment with S0859, an NBCe1 antagonist, blocked the hypoxia-induced increase in T, τ intracellular resting calcium and sodium concentrations, and apoptosis in cardiomyocytes. These findings indicate that NBCe1 overexpression promotes cardiac remodeling by increasing intracellular calcium overload. Therefore, NBCe1 should be a potential target for treatment of cardiac remodeling.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bbadis.2019.165623DOI Listing
March 2020

Lansoprazole alleviates pressure overload-induced cardiac hypertrophy and heart failure in mice by blocking the activation of β-catenin.

Cardiovasc Res 2020 01;116(1):101-113

Department of Cardiology, State Key Laboratory of Organ Failure Research, Nanfang Hospital, Southern Medical University, 1838 Guangzhou Avenue North, Guangzhou 510515, China.

Aims: Proton pump inhibitors (PPIs) are widely used in patients receiving percutaneous coronary intervention to prevent gastric bleeding, but whether PPIs are beneficial for the heart is controversial. Here, we investigated the effects of lansoprazole on cardiac hypertrophy and heart failure, as well as the underlying mechanisms.

Methods And Results: Adult male C57 mice were subjected to transverse aortic constriction (TAC) or sham surgery and then were treated with lansoprazole or vehicle for 5 weeks. In addition, cultured neonatal rat ventricular cardiomyocytes and fibroblasts were exposed to angiotensin II in the presence or absence of lansoprazole. At 5 weeks after TAC, the heart weight/body weight ratio was lower in lansoprazole-treated mice than in untreated mice, as was the lung weight/body weight ratio, while left ventricular (LV) fractional shortening and the maximum and minimum rates of change of the LV pressure were higher in lansoprazole-treated mice, along with less cardiac fibrosis. In cultured cardiomyocytes, lansoprazole inhibited angiotensin II-induced protein synthesis and hypertrophy, as well as inhibiting proliferation of fibroblasts. Lansoprazole decreased myocardial levels of phosphorylated Akt, phosphorylated glycogen synthase kinase 3β, and active β-catenin in TAC mice and in angiotensin II-stimulated cardiomyocytes. After overexpression of active β-catenin or knockdown of H+/K+-ATPase α-subunit, lansoprazole still significantly attenuated myocyte hypertrophy.

Conclusion: Lansoprazole inhibits cardiac remodelling by suppressing activation of the Akt/GSK3β/β-catenin pathway independent of H+/K+-ATPase inhibition, and these findings may provide a novel insight into the pharmacological effects of PPIs with regard to alleviation of cardiac remodelling.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1093/cvr/cvz016DOI Listing
January 2020

MicroRNA-135a-5p promotes neuronal differentiation of pluripotent embryonal carcinoma cells by repressing Sox6/CD44 pathway.

Biochem Biophys Res Commun 2019 02 31;509(2):603-610. Epub 2018 Dec 31.

From the Department of Molecular Neurobiology, Shaanxi Normal University, Xi'an, 710119, China. Electronic address:

MicroRNA-135a-5p has been reported to play a potential role in the generation of new neurons. However, the underlying targets of miR-135a-5p in regulating neuronal differentiation have been poorly understood. Our study recently has uncovered that Sox6 and CD44 genes were significantly downregulated during neuronal differentiation of P19 cells, a multipotent cell type. We then found that Sox6 directly bound to the promoter of CD44. Importantly, we identified Sox6 as a direct target of miR-135a-5p. Additionally, we demonstrated that miR-135a-5p is crucial for the neuronal differentiation of P19 cells. More significantly, we found that Sox6 overexpression could overturn miR-135a-5p-mediated neuronal differentiation and dendrite development. In conclusion, these findings indicated that miR-135a-5p/Sox6/CD44 axis provides an important molecular target mechanism for neurodifferentiation.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bbrc.2018.12.162DOI Listing
February 2019

Phencynonate mediates antidepressant response by activating sirtuin 6-SOD2/Prdx6 pathway.

Biochem Biophys Res Commun 2018 11 9;505(3):898-904. Epub 2018 Oct 9.

Department of Molecular Neurobiology, Shaanxi Normal University, Xi'an, PR China. Electronic address:

Major depression is a highly prevalent disorder with no effective medical treatments available. Recent evidence has shown that sirtuins (SIRTs) signaling has been implicated to play an essential in the pathogenesis of depression. Here in this study, we aimed to investigate the potential role of the phencynonate hydrochloride (PHH) in rat models of chronic unpredictable mild stress (CUMS)-induced depression. SIRT6 expression was up-regulated by PHH via increasing NAD/NADH ratio in the prefrontal cortex. PHH was able to suppress CUMS-induced oxidative stress and enhance the antioxidant capacity and antioxidant proteins activity, such as superoxide dismutase 2 (SOD2) and peroxiredoxin 6 (Prdx6). In vitro study, we found that SIRT6 directly bound to SOD2 and Prdx6 and deacetylated them at Lys68/122 and Lys63/209, which were acetylated by p300/CBP-associated factor (PCAF). Finally, we showed that PHH ameliorated CUMS-induced depressive phenotypes by up-regulating SIRT6 deacetylation activity. In summary, PHH-mediating SIRT6 pathway is required for antidepressant response and PHH can be used as a novel therapeutic to effectively treat depression.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bbrc.2018.10.017DOI Listing
November 2018

Phencynonate mediates antidepressant response by activating sirtuin 6-SOD2/Prdx6 pathway.

Biochem Biophys Res Commun 2018 11 9;505(3):898-904. Epub 2018 Oct 9.

Department of Molecular Neurobiology, Shaanxi Normal University, Xi'an, PR China. Electronic address:

Major depression is a highly prevalent disorder with no effective medical treatments available. Recent evidence has shown that sirtuins (SIRTs) signaling has been implicated to play an essential in the pathogenesis of depression. Here in this study, we aimed to investigate the potential role of the phencynonate hydrochloride (PHH) in rat models of chronic unpredictable mild stress (CUMS)-induced depression. SIRT6 expression was up-regulated by PHH via increasing NAD/NADH ratio in the prefrontal cortex. PHH was able to suppress CUMS-induced oxidative stress and enhance the antioxidant capacity and antioxidant proteins activity, such as superoxide dismutase 2 (SOD2) and peroxiredoxin 6 (Prdx6). In vitro study, we found that SIRT6 directly bound to SOD2 and Prdx6 and deacetylated them at Lys68/122 and Lys63/209, which were acetylated by p300/CBP-associated factor (PCAF). Finally, we showed that PHH ameliorated CUMS-induced depressive phenotypes by up-regulating SIRT6 deacetylation activity. In summary, PHH-mediating SIRT6 pathway is required for antidepressant response and PHH can be used as a novel therapeutic to effectively treat depression.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bbrc.2018.10.017DOI Listing
November 2018

Olmesartan attenuates pressure-overload- or post-infarction-induced cardiac remodeling in mice.

Oncotarget 2018 May 23;9(37):24601-24618. Epub 2017 Dec 23.

State Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.

Either angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor 1 blocker (ARB) attenuates cardiac remodeling. However, the overall molecular modulation of the reversing remodeling process in response to the ACEI or ARB treatment is not yet well determined. In this study, we examined whether gene expressions are modulated by ACEI (temocapril), ARB (olmesartan) or both in a murine model with transverse aortic constriction (TAC) and confirm whether periostin is a target gene of olmesartan in mice with myocardial infarction (MI). We detected 109 genes that were significantly up-regulated in TAC mice and a majority of these were down-regulated in response to temocapril, olmesartan or their combination which significantly attenuated cardiac remodeling at one or four weeks. Real-time RT-PCR demonstrated that olmesartan, temocapril or their combination down-regulated the expression of periostin. In MI mice treated with olmesartan for 4 weeks, the left ventricular end-diastolic and systolic dimensions measured with echocardiography were lower, whereas maximum rate of rise and fall rate of LV pressure (±dp/dt max) were greater, and Azan-staining cardiac fibrotic area was smaller. Furthermore, periostin was upregulated in response to MI, whereas olmesartan blocked this upregulation. Post-MI fibrosis was smaller in periostin knockout adult mice than in wildtype mice, while glycogen synthase kinase 3β was increased and cyclin D1 was decreased in periostin knockout mice. These findings indicate that periostin is a target gene of ARB and olmesartan reverses cardiac remodeling at least partially through the downregulation of periostin.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.18632/oncotarget.23628DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5973849PMC
May 2018

Ethnic Groups Differences in Domestic Recovery after the Catastrophe: A Case Study of the 2008 Magnitude 7.9 Earthquake in China.

Int J Environ Res Public Health 2017 06 2;14(6). Epub 2017 Jun 2.

Key Laboratory of Environmental Change and Natural Disaster of Ministry of Education, Beijing Normal University, Beijing 100875, China.

This research examined the ethnic differences in domestic recovery after the 2008 Wenchuan Earthquake in China. In 2014, 866 valid questionnaires were collected. Han and Qiang & Zang households were analyzed using logistic regression to determine the factors influencing household recovery. It was found that the householder of the Qiang & Zang group played a more important role in household recovery. Different from the Han, females from Qiang & Zang households had negative attitudes on recovery, and Qiang & Zang households did not believe in the effectiveness of public donations for post-quake recovery. The study also showed that local workers in a household were more helpful for household recovery than were migrant workers in a household, regardless of ethnicity. Therefore, the government should create more local jobs in Han and Qiang & Zang households and pay more attention to women in Qiang households. Assistance should be established specifically for the psychological recovery of Qiang women and family recovery projects.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/ijerph14060590DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5486276PMC
June 2017

The Vulnerability of People to Landslides: A Case Study on the Relationship between the Casualties and Volume of Landslides in China.

Int J Environ Res Public Health 2017 02 21;14(2). Epub 2017 Feb 21.

Key Laboratory of Environmental Change and Natural Disaster of Ministry of Education, Beijing Normal University, Beijing 100875, China.

The lack of a detailed landslide inventory makes research on the vulnerability of people to landslides highly limited. In this paper, the authors collect information on the landslides that have caused casualties in China, and established the . 100 landslide cases from 2003 to 2012 were utilized to develop an empirical relationship between the volume of a landslide event and the casualties caused by the occurrence of the event. The error bars were used to describe the uncertainty of casualties resulting from landslides and to establish a threshold curve of casualties caused by landslides in China. The threshold curve was then applied to the landslide cases occurred in 2013 and 2014. The validation results show that the estimated casualties of the threshold curve were in good agreement with the real casualties with a small deviation. Therefore, the threshold curve can be used for estimating potential casualties and landslide vulnerability, which is meaningful for emergency rescue operations after landslides occurred and for risk assessment research.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/ijerph14020212DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5334766PMC
February 2017

Induction of a robust immunity response against novel duck reovirus in ducklings using a subunit vaccine of sigma C protein.

Sci Rep 2016 12 15;6:39092. Epub 2016 Dec 15.

Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Shanghai 200241, China.

Novel duck reovirus (NDRV) disease emerged in China in 2011 and continues to cause high morbidity and about 5.0 to 50% mortality in ducklings. Currently there are no approved vaccines for the virus. This study aimed to assess the efficacy of a new vaccine created from the baculovirus and sigma C gene against NDRV. In this study, a recombinant baculovirus containing the sigma C gene was constructed, and the purified protein was used as a vaccine candidate in ducklings. The efficacy of sigma C vaccine was estimated according to humoral immune responses, cellular immune response and protection against NDRV challenge. The results showed that sigma C was highly expressed in Sf9 cells. Robust humoral and cellular immune responses were induced in all ducklings immunized with the recombinant sigma C protein. Moreover, 100% protection against lethal challenge with NDRV TH11 strain was observed. Summary, the recombinant sigma C protein could be utilized as a good candidate against NDRV infection.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/srep39092DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5156932PMC
December 2016

Induction of a robust immunity response against novel duck reovirus in ducklings using a subunit vaccine of sigma C protein.

Sci Rep 2016 12 15;6:39092. Epub 2016 Dec 15.

Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Shanghai 200241, China.

Novel duck reovirus (NDRV) disease emerged in China in 2011 and continues to cause high morbidity and about 5.0 to 50% mortality in ducklings. Currently there are no approved vaccines for the virus. This study aimed to assess the efficacy of a new vaccine created from the baculovirus and sigma C gene against NDRV. In this study, a recombinant baculovirus containing the sigma C gene was constructed, and the purified protein was used as a vaccine candidate in ducklings. The efficacy of sigma C vaccine was estimated according to humoral immune responses, cellular immune response and protection against NDRV challenge. The results showed that sigma C was highly expressed in Sf9 cells. Robust humoral and cellular immune responses were induced in all ducklings immunized with the recombinant sigma C protein. Moreover, 100% protection against lethal challenge with NDRV TH11 strain was observed. Summary, the recombinant sigma C protein could be utilized as a good candidate against NDRV infection.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/srep39092DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5156932PMC
December 2016

Immunogenicity of virus-like particles containing modified goose parvovirus VP2 protein.

Virus Res 2012 Oct 23;169(1):306-9. Epub 2012 Aug 23.

Division of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, No. 518 Ziyue Road, Minhang District, Shanghai 200241, China.

The major capsid protein VP2 of goose parvovirus (GPV) expressed using a baculovirus expression system (BES) assembles into virus-like particles (VLPs). To optimize VP2 gene expression in Sf9 cells, we converted wild-type VP2 (VP2) codons into codons that are more common in insect genes. This change greatly increased VP2 protein production in Sf9 cells. The protein generated from the codon-optimized VP2 (optVP2) was detected by immunoblotting and an indirect immunofluorescence assay (IFA). Transmission electron microscopy analysis revealed the formation of VLPs. These findings indicate that optVP2 yielded stable and high-quality VLPs. Immunogenicity assays revealed that the VLPs are highly immunogenic, elicit a high level of neutralizing antibodies and provide protection against lethal challenge. The antibody levels appeared to be directly related to the number of GP-Ag-positive hepatocytes. The variation trends for GP-Ag-positive hepatocytes were similar in the vaccine groups. In comparison with the control group, the optVP2 VLPs groups exhibited obviously better responses. These data indicate that the VLPs retained immunoreactivity and had strong immunogenicity in susceptible geese. Thus, GPV optVP2 appears to be a good candidate for the vaccination of goslings.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.virusres.2012.08.009DOI Listing
October 2012
-->