Publications by authors named "Jiang Chang"

661 Publications

Is a Prognostic Marker and Its Expression Is Correlated with MSI in Colorectal Cancer.

Curr Issues Mol Biol 2021 Oct 11;43(3):1529-1547. Epub 2021 Oct 11.

Key Laboratory of Zoonosis Research, Ministry of Education, Institute of Zoonosis, College of Veterinary Medicine, Double-First Class Discipline of Human-Animal Medicine, Jilin University, Changchun 130015, China.

Melanocortin 1 receptor () is thought to be a marker of poor prognosis and a potential target for the treatment of melanoma. Studies have found that promotes several tumor behaviors, including cell proliferation and differentiation, pigment formation, and genome damage repair. Some single-nucleotide polymorphisms (SNPs) of are involved in the occurrence and development of melanoma. A few studies have reported a relationship between and colorectal cancer (CRC). In this research, our objective was to examine expression and SNPs and investigate their correlation with the clinicopathological features of human CRC tissues. We evaluated mRNA expression by performing bioinformatic analyses on human CRC expression datasets. We used Western blotting and RT-qPCR to compare expression in CRC tissues with that in normal tissues, and SNPs in CRC tissues were detected by PCR-direct sequencing (DS). The expression of was significantly decreased in CRC tissues compared with normal tissue, and its expression was negatively associated with expression, expression, and expression, and high expression was significantly associated with microsatellite instability (MSI). SNPs were also associated with the clinicopathological characteristics of CRC; for example, the rs2228479 locus genotype was correlated with status, and the rs885479 locus genotype was correlated with age and T stage. In conclusion, plays a crucial role in the progression of CRC and may be a marker of poor prognosis in CRC.
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http://dx.doi.org/10.3390/cimb43030108DOI Listing
October 2021

Ecological civilization: China's effort to build a shared future for all life on Earth.

Natl Sci Rev 2021 Jul 18;8(7):nwaa279. Epub 2020 Nov 18.

Beyond the Aichi Targets Task Force, IUCN World Commission on Protected Areas.

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http://dx.doi.org/10.1093/nsr/nwaa279DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8310764PMC
July 2021

Hepatocellular carcinoma risk variant modulates lncRNA HLA-DQB1-AS1 expression via a long-range enhancer-promoter interaction.

Carcinogenesis 2021 Oct 19. Epub 2021 Oct 19.

Department of Epidemiology and Biostatistics and Ministry of Education Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Substantial evidence highlighted the critical role of long noncoding RNAs (lncRNA) in driving hepatocarcinogenesis. We hypothesized that functional variants in Genome-wide association studies (GWAS) associated loci might alter the expression levels of lncRNAs and contribute to the development of hepatocellular carcinoma (HCC). Here, we prioritized potentially cis-eQTL-based SNP-lncRNA association together with the physical interaction by the analyses from Hi-C data in GWAS loci of chronic hepatitis B (CHB) and HCC. Subsequently, by leveraging two stage case-control study (1738 hepatitis B (HBV) related HCC cases and 1988 HBV persistent carriers) and biological assays, we identified that rs2647046 was significantly associated with HCC risk (OR = 1.26, 95%CI = 1.11-1.43, P = 4.14×10 -4). Luciferase reporter assays and EMSA assays showed that rs2647046 A allele significantly increased transcriptional activity via influencing TF binding affinity. Allele-specific chromosome conformation capture assays revealed that enhancer with rs2647046 interacted with the HLA-DQB1-AS1 promoter to allele-specifically influence its expression by CTCF-mediated long-range loop. Cell proliferation assays indicated that HLA-DQB1-AS1 is a potential oncogene in HCC. Our study showed HLA-DQB1-AS1 regulated by a causal SNP in a long-range interaction manner conferred the susceptibility to HCC, suggesting an important mechanism of modulating lncRNA expression for risk-associated SNPs in the etiology of HCC.
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http://dx.doi.org/10.1093/carcin/bgab095DOI Listing
October 2021

FOXA1 of regulatory variant associated with risk of breast cancer through allele-specific enhancer in the Chinese population.

Breast Cancer 2021 Oct 11. Epub 2021 Oct 11.

Department of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Background: FOXA1 is a pioneer transcription factor which has been established as a carcinogenic factor and can regulate the expression of downstream target genes in breast cancer. We hypothesized that genetic variants modulating FOXA1 expression might play a role in the risk of breast cancer.

Methods: Physical interaction predicted by PreSTIGE analysis and CHIA-PET data integration with cis-expression quantitative trait loci (cis-eQTL) based SNP-FOXA1 analysis were used to identify potentially regulatory variants modulating the expression of FOXA1. Then, we utilized a case-control study consisting of 855 new diagnosed breast cancer cases and 920 controls in the Chinese population to identify breast cancer associated variants. Biological assays were conducted in breast cancer cell lines to illustrate the effects of associated variants on breast cancer risk.

Results: We identified that rs7160774 G > A variant was associated with lower risk of breast cancer (OR = 0.77, 95% confidence interval = 0.62-0.96, P = 0.022). Biological experiments indicated that rs7160774[A] allele down-regulated the expression of FOXA1 compared to the G allele by influencing transcription factor binding affinity, thus playing an important role in the development of breast cancer.

Conclusion: Our study suggested that the regulatory variant rs7160774 was associated with risk of breast cancer by long-range modulating FOXA1 expression and provided critical insights into pinpoint causal genetic variants.
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http://dx.doi.org/10.1007/s12282-021-01305-1DOI Listing
October 2021

Impact of Inadequate Number of Lymph Nodes Examined on Survival in Stage II Colon Cancer.

Front Oncol 2021 20;11:736678. Epub 2021 Sep 20.

Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.

Background: Inadequate number of lymph nodes examined was not uncommon. We aimed to assess the clinical role of inadequate number of lymph nodes examined in stage II colon cancer.

Methods: The cancer data used in our study were obtained from the SEER (Surveillance, Epidemiology and End Results) program. Using the chi-square test, all the variables obtained in our study were compared based on whether patients had enough (≥12) lymph nodes examined. Kaplan-Meier analysis was used for overall survival (OS) analysis, and log-rank test was applied to compare different N stages with the total number of lymph nodes examined. Multivariate analysis was carried out by creating a Cox proportional hazard model to assess the prognostic roles of different variables.

Results: In total, 80,296 stage II/III colon cancer patients were recruited for our study. N0 stage with <8 lymph nodes examined would present with a worse prognosis compared to N1 stage (5-year OS rates, 51.6% vs. 57.1%, < 0.001). Multivariate analyses indicated that OS of N0 stage with <8 lymph nodes examined was similar to that of N1 stage after adjusting for other recognized prognostic factors [hazard ratios (HRs) = 1.051, 95% confidence intervals (CIs) = 1.014-1.090, = 0.018].

Conclusions: N0 stage with less than eight lymph nodes examined in stage II colon cancer presented with no better OS compared to that of N1 stage. Stage II colon cancer with less than eight lymph nodes examined needed to be given greater emphasis in clinical practice.
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http://dx.doi.org/10.3389/fonc.2021.736678DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8489731PMC
September 2021

Calcium silicate accelerates cutaneous wound healing with enhanced re-epithelialization through EGF/EGFR/ERK-mediated promotion of epidermal stem cell functions.

Burns Trauma 2021 30;9:tkab029. Epub 2021 Sep 30.

Research Center for Tissue Repair and Regeneration affiliated to the Medical Innovation Research Division and Fourth Medical Center of Chinese PLA General Hospital, 100048, Beijing, China.

Background: Human epidermal stem cells (hESCs) play an important role in re-epithelialization and thereby in facilitating wound healing, while an effective way to activate hESCs remains to be explored. Calcium silicate (CS) is a form of bioceramic that can alter cell behavior and promote tissue regeneration. Here, we have observed the effect of CS on hESCs and investigated its possible mechanism.

Methods: Using a mouse full-thickness skin excision model, we explored the therapeutic effect of CS on wound healing and re-epithelialization. , hESCs were cultured with diluted CS ion extracts (CSIEs), and the proliferation, migration ability and stemness of hESCs were evaluated. The effects of CS on the epidermal growth factor (EGF), epidermal growth factor receptor (EGFR) and extracellular signal-related kinase (ERK) signaling pathway were also explored.

Results: , CS accelerated wound healing and re-epithelialization. Immunohistochemistry demonstrated that CS upregulated cytokeratin 19 and integrin β1 expression, indicating that CS improved hESCs stemness. studies confirmed that CS improved the biological function of hESCs. And the possible mechanism could be due to the activation of the EGF/EGFR/ERK signaling pathway.

Conclusion: CS can promote re-epithelialization and improve the biological functions of hESCs via activating the EGF/EGFR/ERK signaling pathway.
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http://dx.doi.org/10.1093/burnst/tkab029DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8484206PMC
September 2021

Organoids derived from neoadjuvant FOLFIRINOX patients recapitulate therapy resistance in pancreatic ductal adenocarcinoma.

Clin Cancer Res 2021 Sep 27. Epub 2021 Sep 27.

Surgery, Erasmus MC

Purpose: We investigated whether organoids can be generated from resected tumors of patients who received eight cycles of neoadjuvant FOLFIRINOX chemotherapy before surgery, and evaluated the sensitivity/resistance of these surviving cancer cells to cancer therapy.

Experimental Design: We generated a library of 10 PDAC organoid lines: five each from treatment-naive and FOLFIRINOX-treated patients. We, first, assessed the histological, genetic, and transcriptional characteristics of the organoids and their matched primary PDAC tissue. Next, the organoids' response to treatment with single agents - 5-FU, irinotecan, and oxaliplatin - of the FOLFIRINOX regimen as well as combined regimen was evaluated. Finally, global mRNA-seq analyses were performed to identify FOLFIRINOX resistance pathways.

Results: All 10 patient-derived PDAC organoids recapitulate histological, genetic, and transcriptional characteristics of their primary tumor tissue. Neoadjuvant FOLFIRINOXtreated organoids display resistance to FOLFIRINOX (5/5), irinotecan (5/5) and oxaliplatin (4/5) when compared to treatment-naive organoids (FOLFIRINOX: 1/5, irinotecan: 2/5, oxaliplatin: 0/5). 5-FU treatment responses between naive and treated organoids were similar. Comparative global transcriptome analysis of treatment-naive and FOLFIRINOX samples - in both organoids and corresponding matched tumor tissues - uncovered modulated pathways mainly involved in genomic instability, energy metabolism, and innate immune system.

Conclusion: Resistance development in neoadjuvant FOLFIRINOX organoids, recapitulating their primary tumor resistance, suggests continuation of FOLFIRINOX therapy as an adjuvant treatment may not be advantageous for these patients. Gene expression profiles of PDAC organoids identify targetable pathways involved in chemoresistance development upon neoadjuvant FOLFIRINOX treatment, thus opening up combination therapy possibilities.
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http://dx.doi.org/10.1158/1078-0432.CCR-21-1681DOI Listing
September 2021

Radiosensitivity-Specific Proteomic and Signaling Pathway Network of Non-Small Cell Lung Cancer (NSCLC).

Int J Radiat Oncol Biol Phys 2021 Sep 8. Epub 2021 Sep 8.

Department of Radiation Oncology, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China. Electronic address:

Purpose: An unmet clinical need in non-small cell lung cancer (NSCLC) management is the accurate prediction of radiation response in patients receiving radical radiation therapy. We explored the intrinsic radiosensitivity of NSCLC from the proteomic profiles of NSCLC cell lines and paraffin-embedded human samples.

Methods And Materials: To uncover radiosensitivity-specific proteomic and signaling pathways, we performed quantitative proteomics by data-independent acquisition mass spectrometry assay on 29 human NSCLC cell lines and 13 paraffin-embedded human NSCLC samples. We validated closely interacting radioresistant proteins by western blotting, immunofluorescence, real-time quantitative polymerase chain reaction in NSCLC cell lines, and immunohistochemistry in paraffin-embedded human samples. We validated the functions of 3 key hub proteins by lentivirus transfection, clonogenic survival assay, and flow cytometry.

Results: The proteomic profiling of NSCLC showed that the intrinsic radiosensitivity of NSCLC is mainly modulated by signaling pathways of proteoglycans in cancer, focal adhesion, and regulation of the actin cytoskeleton. We identified 71 differentially expressed proteins and validated 8 closely interacting proteins as radioresistant proteins of NSCLC. Moreover, we also validated the functionality of integrin-linked protein kinase, p21-activated kinase 1, and Ras GTPase-activating-like protein IQGAP1 in the radiation response of NSCLC cell lines. Finally, with the NSCLC radiosensitivity-specific proteins, we delineated the atlas network of NSCLC radiosensitivity-related signaling pathways.

Conclusions: Radiosensitivity-specific proteins could guide individualized radiation therapy in clinical practice by predicting the radiation response of patients with NSCLC. Moreover, the NSCLC radiosensitivity-related signaling pathway atlas could guide further exploration of the underlying mechanism.
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http://dx.doi.org/10.1016/j.ijrobp.2021.08.041DOI Listing
September 2021

Rectal adenocarcinoma with multifocal osteoid differentiation.

Asian J Surg 2021 Sep 4. Epub 2021 Sep 4.

Shanxi Province Cancer Hospital, Gastroenterology Ward One, 030013, China. Electronic address:

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http://dx.doi.org/10.1016/j.asjsur.2021.08.057DOI Listing
September 2021

Urinary bisphenol A and its interaction with CYP17A1 rs743572 are associated with breast cancer risk.

Chemosphere 2021 Aug 12;286(Pt 3):131880. Epub 2021 Aug 12.

Department of Epidemiology and Biostatistics and Ministry of Education Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address:

Objective: Bisphenol A (BPA), a common endocrine disrupter, can be activated by cytochrome P450 (CYP) metabolizing enzymes and might influence the development of breast cancer (BC). We hypothesized that BPA could interact with CYP genes, synergistically contributing to the BC risk.

Methods: Urinary BPA was measured in a total of 302 newly diagnosed BC patients and 302 healthy controls by ultra-high performance liquid chromatography-high resolution mass spectrometry. A set of seven CYP gene polymorphisms was genotyped by using the Sequenom MassARRAY system. A multivariate logistic regression model was used to assess the associations of BPA and BPA-SNP interaction with BC risk.

Results: BC patients had a higher urinary BPA concentration than healthy individuals (P < 0.001). Each 1-unit increase in log-transformed urinary BPA was associated with a 54 % increased BC risk [95 % confidence interval (CI), 1.34-1.77, P < 0.001]. Individuals with the CYP19A1 rs1902580 GA + AA genotype showed a significantly higher BC risk than those with the GG genotype (OR = 1.45, 95 % CI, 1.01-2.09, P < 0.05). A significant BPA-CYP17A1 rs743572 interaction was found to be associated with a higher risk of BC (P = 0.020). Compared with low-BPA individuals carrying CYP17A1 rs743572 GG genotypes, high-BPA individuals with the GA + AA genotype had a higher BC risk, with an odds ratio of 2.49 (95 % CI, 1.52-4.13, P < 0.05).

Conclusions: The positive association of BPA exposure with BC risk might be modified by CYP17A1 rs743572, providing evidence for the interaction effect of environment-genes on the etiology of BC.
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http://dx.doi.org/10.1016/j.chemosphere.2021.131880DOI Listing
August 2021

Lower Serum Angiotensin-Converting Enzyme Level in Relation to Hyperinflammation and Impaired Antiviral Immune Response Contributes to Progression of COVID-19 Infection.

Infect Dis Ther 2021 Aug 13. Epub 2021 Aug 13.

Department and Institute of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Introduction: As a homologue of the angiotensin-converting enzyme (ACE), angiotensin-converting enzyme 2 (ACE2) has been identified as the main receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) invasion. We aimed to investigate the role of serum ACE in predicting the coronavirus disease 2019 (COVID-19) disease progression and the underlying mechanisms.

Methods: We retrospectively enrolled 120 patients with confirmed COVID-19 who underwent serum ACE detection on admission. The clinical characteristics and laboratory findings during hospitalization were evaluated dynamically to identify the potential risk factors for disease progression.

Results: ACE level was demonstrated as one of the independent risk factors. Patients with ACE level ≤ 33.5 U/L showed a higher cumulative virus RNA detection rate, elevated pro-inflammatory mediators levels, declined lymphocyte count, and decreased SARS-CoV-2-specific antibodies than those with ACE level > 33.5 U/L.

Conclusion: Lower serum ACE levels in relation to delayed virus elimination, hyperinflammatory condition, and impaired host antiviral immune responses contribute to disease progression of COVID-19.
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http://dx.doi.org/10.1007/s40121-021-00513-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8361819PMC
August 2021

Genetic association study of childhood aggression across raters, instruments, and age.

Transl Psychiatry 2021 07 30;11(1):413. Epub 2021 Jul 30.

Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.

Childhood aggressive behavior (AGG) has a substantial heritability of around 50%. Here we present a genome-wide association meta-analysis (GWAMA) of childhood AGG, in which all phenotype measures across childhood ages from multiple assessors were included. We analyzed phenotype assessments for a total of 328 935 observations from 87 485 children aged between 1.5 and 18 years, while accounting for sample overlap. We also meta-analyzed within subsets of the data, i.e., within rater, instrument and age. SNP-heritability for the overall meta-analysis (AGG) was 3.31% (SE = 0.0038). We found no genome-wide significant SNPs for AGG. The gene-based analysis returned three significant genes: ST3GAL3 (P = 1.6E-06), PCDH7 (P = 2.0E-06), and IPO13 (P = 2.5E-06). All three genes have previously been associated with educational traits. Polygenic scores based on our GWAMA significantly predicted aggression in a holdout sample of children (variance explained = 0.44%) and in retrospectively assessed childhood aggression (variance explained = 0.20%). Genetic correlations (r) among rater-specific assessment of AGG ranged from r = 0.46 between self- and teacher-assessment to r = 0.81 between mother- and teacher-assessment. We obtained moderate-to-strong rs with selected phenotypes from multiple domains, but hardly with any of the classical biomarkers thought to be associated with AGG. Significant genetic correlations were observed with most psychiatric and psychological traits (range [Formula: see text]: 0.19-1.00), except for obsessive-compulsive disorder. Aggression had a negative genetic correlation (r = ~-0.5) with cognitive traits and age at first birth. Aggression was strongly genetically correlated with smoking phenotypes (range [Formula: see text]: 0.46-0.60). The genetic correlations between aggression and psychiatric disorders were weaker for teacher-reported AGG than for mother- and self-reported AGG. The current GWAMA of childhood aggression provides a powerful tool to interrogate the rater-specific genetic etiology of AGG.
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http://dx.doi.org/10.1038/s41398-021-01480-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8324785PMC
July 2021

A Combined Network Pharmacology and Molecular Docking Approach to Investigate Candidate Active Components and Multitarget Mechanisms of Hemerocallis Flowers on Antidepressant Effect.

Evid Based Complement Alternat Med 2021 30;2021:7127129. Epub 2021 Jun 30.

School of Functional Food and Wine, Shenyang Pharmaceutical University, Wenhua Road 103, Shenyang 110016, China.

Objective: The purpose of our research is to systematically explore the multiple mechanisms of Flowers (HF) on depressive disorder (DD).

Methods: The components of HF were searched from the literature. The targets of components were obtained from PharmMapper. After that, Cytoscape software was used to build a component-target network. The targets of DD were collected from DisGeNET, PharmGKB, TTD, and OMIM. Protein-protein interactions (PPIs) among the DD targets were executed to screen the key targets. Afterward, the GO and KEGG pathway enrichment analysis were performed by the KOBAS database. A compound-target-KEGG pathway network was built to analyze the key compounds and targets. Finally, the potential active substances and targets were validated by molecular docking.

Results: A total of 55 active compounds in HF, 646 compound-related targets, and 527 DD-related targets were identified from public databases. After treated with PPI, 219 key targets of DD were acquired. The gene enrichment analysis suggested that HF probably benefits DD patients by modulating pathways related to the nervous system, endocrine system, amino acid metabolism, and signal transduction. The network analysis showed the critical components and targets of HF on DD. Results of molecular docking increased the reliability of this study.

Conclusions: It predicted and verified the pharmacological and molecular mechanism of HF against DD from a holistic perspective, which will also lay a foundation for further experimental research and rational clinical application of DD.
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http://dx.doi.org/10.1155/2021/7127129DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8266453PMC
June 2021

Sirt3 promotes the autophagy of HK‑2 human proximal tubular epithelial cells via the inhibition of Notch‑1/Hes‑1 signaling.

Mol Med Rep 2021 Sep 19;24(3). Epub 2021 Jul 19.

Department of Nephrology, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, P.R. China.

Diabetic nephropathy (DN) is a predominant cause of end‑stage renal disease. The impairment of the autophagy of human renal tubular epithelial cells (HK‑2 cells) is involved in the pathogenic mechanisms of DN. Sirtuin (Sirt)3 regulates the scavenging of damaged organelles and maintains energy balance. The present study aimed to examine the protective effects of Sirt3 on HK‑2 cells stimulated by high glucose (HG). HK‑2 cells were cultured in normal glucose (NG), HG or hyperosmotic medium. The viability of the HK‑2 cells was detected using a Cell Counting Kit‑8 assay. The expression and localization of Sirt3 were detected via immunofluorescence. Following transfection with an overexpression plasmid, the expression levels of key components in the Notch homolog 1 (Notch‑1)/hairy and enhancer of split‑1 (Hes‑1) pathway and those of the autophagy‑related proteins, Beclin‑1, LC‑3II and p62, were measured by western blot analysis and reverse transcription‑quantitative PCR (RT‑qPCR). As the Notch‑1/Hes‑1 pathway was inhibited, the expression levels of Beclin‑1, LC‑3II and p62 were also examined at transcriptional and translational level. It was found that prolonged culture in HG medium markedly reduced cell viability compared with the cells cultured in NG or in NG + mannitol, an effect that was aggravated with the increasing duration of culture. HG was capable of inhibiting the expression levels of Beclin‑1, LC‑3II and Sirt3, and upregulating p62 and the Notch‑1/Hes‑1 pathway, as verified by western blot analysis and RT‑qPCR. The results of immunofluorescence staining revealed that HG decreased Sirt3 expression. Sirt3 reversed the HG‑induced inhibition of the expression of Beclin‑1 and LC‑3II and the upregulation of p62. Moreover, Sirt3 reversed the HG‑induced inhibition of the Notch‑1/Hes‑1 signaling pathway. However, this autophagy‑promoting effect of Sirt3 was counteracted by the Notch‑1/Hes‑1 pathway activator. On the whole, the present study demonstrated that Sirt3 promoted the autophagy of HK‑2 cells, at least partly, via the downregulation of Notch‑1/Hes‑1.
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http://dx.doi.org/10.3892/mmr.2021.12273DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8281085PMC
September 2021

Colorectal cancer risk variant rs7017386 modulates two oncogenic lncRNAs expression via ATF1-mediated long-range chromatin loop.

Cancer Lett 2021 Oct 15;518:140-151. Epub 2021 Jul 15.

Department of Epidemiology and Biostatistics, And the Ministry of Education Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address:

The activating transcription factor 1 (ATF1) has been identified as a vital pathogenic factor in the progression of colorectal cancer (CRC), whiles, the precise regulatory mechanisms remain elusive. Here, we comprehensively characterized the ATF1 cistrome by RNA-seq and ChIP-seq assays in CRC cell lines. As the results, we identified 358 genes differentially regulated and 15,029 ATF1 binding sites and demonstrated that ATF1 was widely involved in major signaling pathways in CRC, such as Wnt, TNF, Jak-STAT. Subsequently, by the expression quantitative trait loci (eQTL) analyses, we found that rs7017386 was associated with the expression of CCAT1 and PVT1 in the Wnt pathway. By a two-stage population study with 6,131 CRC cases and 10,022 healthy controls, we identified the variant was associated with CRC risk. Mechanistically, we found rs7017386 allele-specifically enhanced the binding affinity of ATF1 and promoted the expressions of PVT1 and CCAT1, via forming a long-range chromatin loop. Moreover, those two lncRNAs could synergistically facilitate c-Myc expression to activate the Wnt pathway in CRC progression. Our findings not only demonstrated the transcriptomic profiling of ATF1 in CRC, but also provided important clues for the etiology of CRC.
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http://dx.doi.org/10.1016/j.canlet.2021.07.021DOI Listing
October 2021

Epidemiological investigation of urinary incontinence in peri- and postpartum women from Nanjing, China.

Low Urin Tract Symptoms 2021 Oct 8;13(4):481-489. Epub 2021 Jul 8.

Department of Gynecology and Obstetrics, Women's Hospital of Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital, Nanjing, China.

Objectives: We aimed to determine the prevalence of urinary incontinence (UI) during the peri- and postpartum period in women from Nanjing, China, and estimate its risk factors.

Methods: From January to December 2018, a total of 6500 postpartum women were enrolled and asked to complete the questionnaires. Of these, 6370 (98%) women returned the questionnaires with valid responses. Additional data were collected, including age, height, weight, gestation time and parity, and neonatal weight. The International Consultation on Incontinence Questionnaire-Urinary Incontinence Short Form was used. Surface electromyography (sEMG) and a biofeedback training system were used as a testing platform, and PESEMG values were obtained.

Results: The prevalence of UI during pregnancy and at 6 weeks postpartum in women was 29.76% and 12.50%, respectively. The prevalence of stress UI (SUI), urge UI (UUI), mixed UI (MUI), and other types of UI that developed during pregnancy was 25.48%, 1.66%, 1.65%, and 0.97%, respectively. The prevalence of SUI, UUI, MUI, and other types of UI at 6 weeks postpartum was 8.49%, 2.07%, 1.16%, and 0.77%, respectively. Multivariate analysis showed that advanced age, greater postpartum body mass index (BMI), macrosomia, multiparity, and vaginal delivery were risk factors of postpartum UI. Women with mild degree of UI in pregnancy, those who had undergone cesarean section, and those without UI before pregnancy were relieved from UI at 6 weeks postpartum.

Conclusions: The rate of UI in peri- and postpartum women from Nanjing is consistent across China. The most common type of UI was SUI, with many risk factors affecting its occurrence. Advanced age, greater postpartum BMI, multiparity, macrosomia, and vaginal delivery might be the main risk factors of UI in postpartum women.
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http://dx.doi.org/10.1111/luts.12399DOI Listing
October 2021

A bibliometric analysis of the application of procalcitonin in patients in the intensive care unit.

Ann Palliat Med 2021 06 21;10(6):6367-6378. Epub 2021 Jun 21.

Outpatient Health Examination Center, Shaanxi Provincial People's Hospital, Xi'an, China.

Background: Patients in the intensive care unit (ICU) often have serious infections, and anti-infection treatment is vital for these patients. Procalcitonin (PCT) is often used to identify bacterial infections and monitor the effectiveness of anti-infection treatments. This study aims to analyze the current research hotspots of the application of PCT in ICU patients, and to suggest future research directions.

Methods: The Science Citation Index Expanded (SCI-EXPANDED) database in the Web of Science Core Collection (WOSCC) was used as the data source to search literature from 1995 to February 6, 2021. The search strategy was subject term = procalcitonin AND Web of Science categories = Critical Care Medicine. Using CiteSpace software, literature on the application of PCT in ICU patients was analyzed.

Results: A total of 1,243 papers, including 665 (53.5%) original articles, 87 (7.0%) reviews, 93 (7.5%) letters, 297 (23.9%) conference abstracts, and 101 (8.1%) other articles, were analyzed. The citation frequency was 40,442, the h-index was 96, and the average number of citations per item was 32.54. Research was mainly from the United States, Germany, France, and Spain, amongst others. The research institutions were mainly Univ Basel Hosp, Univ Pittsburgh, and Univ Hosp Geneva. Authors including Schuetz P made more contributions. Critical Care Medicine, Intensive Care Medicine, and Critical Care were important journals in this field of research. The keywords with the highest frequency were PCT, sepsis, and infection, and the more central ones were PCT, inflammation, septic shock, and C-reactive protein. The keywords with the strongest citation bursts were PCT, cytokine, and serum.

Conclusions: Papers are mainly published in critical care medical journals. The countries, institutions, and authors that carry out research are relatively limited. The current hot spots are still inflammation, infection, and shock, especially the management and prognosis prediction of critically ill patients.
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http://dx.doi.org/10.21037/apm-21-895DOI Listing
June 2021

CYB561A3 is the Key Lysosomal Iron Reductase Required for Burkitt B-cell Growth and Survival.

Blood 2021 Jul 7. Epub 2021 Jul 7.

Broad Institute of Harvard And MIT, United States.

Epstein-Barr virus (EBV) causes endemic Burkitt lymphoma, the leading childhood cancer in sub-Saharan Africa. Burkitt cells retain aspects of germinal center B-cell physiology with MYC-driven B-cell hyperproliferation, yet little is presently known about their iron metabolism. CRISPR/Cas9 analysis highlighted the little studied ferrireductase CYB561A3 as critical for Burkitt proliferation, but not for that of closely related EBV-transformed lymphoblastoid cells or nearly all other Cancer Dependency Map cell lines. Burkitt CYB561A3 knockout induced profound iron starvation, despite ferritinophagy and plasma membrane transferrin upregulation. Elevated concentrations of ascorbic acid, a key CYB561 family electron donor or the labile iron source ferrous citrate rescued Burkitt CYB561A3 deficiency. CYB561A3 knockout caused catastrophic lysosomal and mitochondrial damage and impaired mitochondrial respiration. By contrast, lymphoblastoid B-cells with the transforming EBV latency III program were instead dependent on the STEAP3 ferrireductase. These results highlight CYB561A3 it as an attractive therapeutic Burkitt lymphoma target.
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http://dx.doi.org/10.1182/blood.2021011079DOI Listing
July 2021

Aberrant MCM10 SUMOylation induces genomic instability mediated by a genetic variant associated with survival of esophageal squamous cell carcinoma.

Clin Transl Med 2021 06;11(6):e485

Department of Epidemiology and Biostatistics, Key Laboratory for Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan, China.

Background: Esophageal squamous cell carcinoma (ESCC) is one of the common gastrointestinal malignancy with an inferior prognosis outcome. DNA replication licensing aberration induced by dysregulation of minichromosome maintenance proteins (MCMs) causes genomic instability and cancer metastasis. SUMOylation modification plays a pivotal role in regulation of genomic integrity, while its dysregulation fueled by preexisting germline variants in cancers remains poorly understood.

Methods: Firstly, we conducted two-stage survival analysis consisting of an exome-wide association study in 904 ESCC samples and another independent 503 ESCC samples. Then, multipronged functional experiments were performed to illuminate the potential biological mechanisms underlying the promising variants, and MCM10 influences the ESCC progression. Finally, we tested the effects of MCM10 inhibitors on ESCC cells.

Results: A germline variant rs2274110 located at the exon 15 of MCM10 was identified to be significantly associated with the prognosis of ESCC patients. Individuals carrying rs2274110-AA genotypes confer a poor survival (hazard ratio = 1.61, 95% confidence interval = 1.35-1.93, p = 1.35 × 10 ), compared with subjects carrying rs2274110-AG/GG genotypes. Furthermore, we interestingly found that the variant can increase SUMOylation levels at K669 site (Lys[K]699Arg[R]) of MCM10 protein mediated by SUMO2/3 enzymes, which resulted in an aberrant overexpression of MCM10. Mechanistically, aberrant overexpression of MCM10 facilitated the proliferation and metastasis abilities of ESCC cells in vitro and in vivo by inducing DNA over-replication and genomic instability, providing functional evidence to support our population finding that high expression of MCM10 is extensively presented in tumor tissues of ESCC and correlated with inferior survival outcomes of multiple cancer types, including ESCC. Finally, MCM10 inhibitors Suramin and its analogues were revealed to effectively block the metastasis of ESCC cells.

Conclusions: These findings not only demonstrate a potential biological mechanism between aberrant SUMOylation, genomic instability and cancer metastasis, but also provide a promising biomarker aiding in stratifying ESCC individuals with different prognosis, as well as a potential therapeutic target MCM10.
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http://dx.doi.org/10.1002/ctm2.485DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8236122PMC
June 2021

Bisphenol A exposure, interaction with genetic variants and colorectal cancer via mediating oxidative stress biomarkers.

Environ Pollut 2021 Oct 23;287:117630. Epub 2021 Jun 23.

Department of Epidemiology and Biostatistics and Ministry of Education Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Bisphenol A (BPA) may induce oxidative stress as well as the toxicity of colon cancer cells. We hypothesized that BPA exposure and interactions with genetic variants might be associated with colorectal cancer (CRC) risk, and the association might be partly mediated by oxidative stress. We measured urinary BPA and three oxidative stress markers [8-iso-prostaglandinF (8-isoPGF), 8-hydroxydeoxyguanosine (8-OHdG) and 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA)] in 275 new CRC cases and 538 healthy controls. A set of 25 genetic variations in 12 candidate DNA repair genes and 5 metabolic enzyme genes were genotyped by Sequenom MassARRAY approach. In multivariable logistic regression, significant positive associations of CRC risk with BPA, 8-OHdG and HNE-MA were observed. Additionally, 8-OHdG, HNE-MA and 8-isoPGF were significantly positively associated with BPA (P < 0.05). The mediation analysis showed BPA-associated HNE-MA significantly mediated 11.81% of the effect of BPA on CRC risk. Moreover, BPA was found to interact with ERCC5 rs17655 and rs2296147 (both P < 0.05) to increase CRC risk. In brief, our results suggested BPA was associated with CRC risk and the positive association of BPA with CRC risk might be partly mediated by the oxidative stress HNE-MA. BPA might interact with ERCC5 rs17655 and rs2296147 to increase CRC risk.
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http://dx.doi.org/10.1016/j.envpol.2021.117630DOI Listing
October 2021

Increased diagnosis of enlarged vestibular aqueduct by multiplex PCR enrichment and next-generation sequencing of the SLC26A4 gene.

Mol Genet Genomic Med 2021 Aug 25;9(8):e1734. Epub 2021 Jun 25.

The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Background: The enlarged vestibular aqueduct (EVA) is the commonest malformation of inner ear accompanied by sensorineural hearing loss in children. Three genes SLC26A4, FOXI1, and KCNJ10 have been associated with EVA, among them SLC26A4 being the most common. Yet, hotspot mutation screening can only diagnose a small number of patients.

Methods: Thus, in this study, we designed a new molecular diagnosis panel for EVA based on multiplex PCR enrichment and next-generation sequencing of the exon and flanking regions of SLC26A4. A total of 112 hearing loss families with EVA were enrolled and the pathogenicity of the rare variants detected was interpreted according to the American College of Medical Genetics and Genomics (ACMG) guidelines.

Results: Our results showed that 107/112 (95.54%) families carried SLC26A4 biallelic mutations, 4/112 (3.57%) carried monoallelic variants, and 1/112 (0.89%) had none variant, resulting in a diagnostic rate of 95.54%. A total of 49 different variants were detected in those patients and we classified 30 rare variants as pathogenic/likely pathogenic, of which 13 were not included in the Clinvar database.

Conclusion: Our diagnostic panel has an increased diagnostic yield with less cost, and the curated list of pathogenic variants in the SLC26A4 gene can be directly used to aid the genetic counseling to patients.
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http://dx.doi.org/10.1002/mgg3.1734DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8404235PMC
August 2021

Dissemination of IncFII plasmids carrying fosA3 and bla in clinical isolates of Salmonella enteritidis.

Zoonoses Public Health 2021 Nov 4;68(7):760-768. Epub 2021 Jun 4.

Department of Food Science & Technology, School of Agriculture and Biology, State Key Lab of Microbial Metabolism, Shanghai Jiao Tong University, Shanghai, China.

Multidrug-resistant Salmonella Enteritidis (S. Enteritidis) isolates have become a significant threat to public health, and fosfomycin has been proposed as one of the therapeutic antibiotics for serious infections by resistant pathogens. In this study, a total of 501 clinical S. Enteritidis isolates were screened and 14 (2.8%) isolates exhibited resistance to fosfomycin (MIC ≥ 1,024 μg/mL) as well as ceftriaxone (MIC ≥ 128 μg/mL). The fosA3 gene was identified in these 14 isolates. The fosA3 gene that co-transferred with bla was observed on the IncFII plasmids with sizes of ~ 78 (n = 7) or ~ 111 (n = 2) kbp in 9 transconjugants. The fosA3-bearing plasmid p12367A is 111,764 bp in length and possessed a typical IncFII backbone. A 7.6-kbp multidrug resistance region (MRR) was identified in p12367A, which was comprised of fosA3 and bla genes interspersed with ΔISEcp1 and three copies of IS26. Two typical antibiotic resistance determinants (IS26-orf3-orf2-orf1-fosA3-IS26 and IS26-orf477-bla -ΔISEcp1-IS26) shared one IS26 in the MRR. The genetic arrangement of the MRR may have resulted from the stepwise integration of IS26 mobile elements via homologous recombination. Horizontal transfer of IncFII plasmids might contribute to the dissemination of fosA3 and bla resistance genes in S. Enteritidis interspecies. These findings underline further challenges for the prevention and treatment of Enterobacteriaceae infections posed by epidemic IncFII plasmids bearing fosA3-bla .
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http://dx.doi.org/10.1111/zph.12825DOI Listing
November 2021

Genetic variants associated with expression of contribute to the risk of head and neck cancer in Chinese population.

J Med Genet 2021 Mar 5. Epub 2021 Mar 5.

Department of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China

Background: Squamous cell carcinoma of the head and neck (SCCHN) is one of the most common cancers worldwide and includes cancers arising from the oral cavity, pharynx and larynx. Genome-wide association studies have found several genetic variants related to the risk of SCCHN; however, they could only explain a small fraction of the heritability. Thus, more susceptibility loci associated with SCCHN need to be identified.

Methods: An association study was conducted by genotyping 555 patients with SCCHN and 1367 controls in a Chinese population. Single-variant association analysis was conducted on 63 373 SNPs, and the promising variants were then confirmed by a two-stage validation with 1875 SCCHN cases and 4637 controls. Bioinformatics analysis and functional assays were applied to uncover the potential pathogenic mechanism of the promising variants and genes associated with SCCHN.

Results: We first identified three novel genetic variants significantly associated with the risk of SCCHN (p=7.45×10 for rs2517611 at 6p22.1, p=1.76×10 for rs2524182 at 6p21.33 and p=2.17×10 for rs3131018 at 6p21.33). Further analysis and biochemical assays showed that rs3094187, which was in a region in high linkage disequilibrium with rs3131018, could modify expression by regulating the binding affinity of the transcription factor to the promoter of . In addition, experiments revealed that the inhibition of may affect several important pathways involved in tumourigenesis and attenuate the cell proliferation and migration of SCCHN.

Conclusion: These findings offer important evidence that functional genetic variants could contribute to development of SCCHN and that may function as a putative susceptibility gene for SCCHN.
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http://dx.doi.org/10.1136/jmedgenet-2020-107410DOI Listing
March 2021

MicroRNA-182 improves spinal cord injury in mice by modulating apoptosis and the inflammatory response via IKKβ/NF-κB.

Lab Invest 2021 09 31;101(9):1238-1253. Epub 2021 May 31.

Department of Orthopedics, Zhongshan Hospital, Fudan University, Shanghai, China.

Spinal cord injury (SCI) is one common neurological condition which involves primary injury and secondary injury. Neuron inflammation and apoptosis after SCI is the most important pathological process of this disease. Here, we tried to explore the influence and mechanism of miRNAs on the neuron inflammatory response and apoptosis after SCI. First, by re-analysis of Gene Expression Omnibus dataset (accession GSE19890), miR-182 was selected for further study because of its suppressive effects on the inflammatory response in the various types of injuries. Functional experiments demonstrated that miR-182 overexpression promoted functional recovery, reduced histopathological changes, and alleviated spinal cord edema in mice. It was also observed that miR-182 overexpression reduced apoptosis and attenuated the inflammatory response in spinal cord tissue, as evidenced by the reduction of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β, and the induction of IL-10. Using a lipopolysaccharide (LPS)-induced SCI model in BV-2 cells, we found that miR-182 was downregulated in the BV-2 cells following LPS stimulation, and upregulation of miR-182 improved LPS-induced cell damage, as reflected by the inhibition of apoptosis and the inflammatory response. IκB kinase β (IKKβ), an upstream target of the NF-κB pathway, was directly targeted by miR-182 and miR-182 suppressed its translation. Further experiments revealed that overexpression of IKKβ reversed the anti-apoptosis and anti-inflammatory effects of miR-182 in LPS stimulated BV-2 cells. Finally, we found that miR-182 overexpression blocked the activation of the NF-κB signaling pathway in vitro and in vivo, as demonstrated by the downregulation of phosphorylated (p‑) IκB-α and nuclear p-p65. Taken together, these data indicate that miR-182 improved SCI-induced secondary injury through inhibiting apoptosis and the inflammatory response by blocking the IKKβ/NF-κB pathway. Our findings suggest that upregulation of miR-182 may be a novel therapeutic target for SCI.
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http://dx.doi.org/10.1038/s41374-021-00606-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8367816PMC
September 2021

Mutation of SlARC6 leads to tissue-specific defects in chloroplast development in tomato.

Hortic Res 2021 Jun 1;8(1):127. Epub 2021 Jun 1.

College of Horticulture, FAFU-UCR Joint Center and Fujian Provincial Key Laboratory of Haixia Applied Plant Systems Biology, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.

The proliferation and development of chloroplasts are important for maintaining the normal chloroplast population in plant tissues. Most studies have focused on chloroplast maintenance in leaves. In this study, we identified a spontaneous mutation in a tomato mutant named suffulta (su), in which the stems appeared albinic while the leaves remained normal. Map-based cloning showed that Su encodes a DnaJ heat shock protein that is a homolog of the Arabidopsis gene AtARC6, which is involved in chloroplast division. Knockdown and knockout of SlARC6 in wild-type tomato inhibit chloroplast division, indicating the conserved function of SlARC6. In su mutants, most mesophyll cells contain only one or two giant chloroplasts, while no chloroplasts are visible in 60% of stem cells, resulting in the albinic phenotype. Compared with mature tissues, the meristem of su mutants suggested that chloroplasts could partially divide in meristematic cells, suggesting the existence of an alternative mechanism in those dividing cells. Interestingly, the adaxial petiole cells of su mutants contain more chloroplasts than the abaxial cells. In addition, prolonged lighting can partially rescue the albinic phenotypes in su mutants, implying that light may promote SlACR6-independent chloroplast development. Our results verify the role of SlACR6 in chloroplast division in tomato and uncover the tissue-specific regulation of chloroplast development.
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http://dx.doi.org/10.1038/s41438-021-00567-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8167136PMC
June 2021

Silencing of Long Noncoding RNA Growth Arrest-Specific 5 Alleviates Neuronal Cell Apoptosis and Inflammatory Responses Through Sponging microRNA-93 to Repress PTEN Expression in Spinal Cord Injury.

Front Cell Neurosci 2021 14;15:646788. Epub 2021 May 14.

Department of Orthopedics, Zhongshan Hospital, Fudan University, Shanghai, China.

A secondary injury induced by a spinal cord injury (SCI) remains the main cause of devastating neural dysfunction; therefore, it has been the subject of focused research for many years. Long noncoding RNA (lncRNA) has been found to participate in the SCI process, and this finding presents a high potential for diagnosis and treatment; however, the role of lncRNA in a secondary injury induced by SCI remains unclear. The aim of this study was to investigate the regulatory effect of lncRNA growth arrest-specific transcript 5 (GAS5) in secondary injury during SCI. The SCI mice model and hypoxic cellular model were established to research the roles of lncRNA GAS5 during SCI. Reverse transcription quantitative polymerase chain reaction (qRT-PCR) was conducted to determine the expression levels of microR-93 (miR-93) and lncRNA GAS5. Western blot analysis of the apoptosis regulator protein and terminal deoxynucleotidyl transferase dUTP nick end labeling assay was conducted to evaluate neuron cell apoptosis. Basso, Beattie, and Bresnahan (BBB) scores were calculated to assess neurological function. Flow cytometry was used to determine neuron cell apoptosis. The associations among GAS5, miR-93, and the phosphatase and tensin homolog (PTEN) were disclosed using RNA immunoprecipitation (RIP) assay, RNA pulldown assay, and dual-luciferase reporter assay. QRT-PCR demonstrated that GAS5 was significantly upregulated in both the SCI mice and hypoxic cellular models. GAS5 knockdown suppressed neuron cell apoptosis and inflammatory response in the SCI mice model. Further studies have indicated that GAS5 functions as a competing endogenous RNA (ceRNA) by sponging miR-93 in neuronal cells. In addition, PTEN was a target of miR-93, and GAS5 knockdown exhibited its anti-apoptotic and anti-inflammatory effects through the miR-93/PTEN axis. These findings suggest that the GAS5/miR-93/PTEN axis may be a promising therapeutic target for SCI.
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http://dx.doi.org/10.3389/fncel.2021.646788DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8163226PMC
May 2021

Maternal RND3/RhoE deficiency impairs placental mitochondrial function in preeclampsia by modulating the PPARγ-UCP2 cascade.

FASEB J 2021 06;35(6):e21555

Department of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Preeclampsia (PE) is a life-threatening disease of pregnant women associated with severe hypertension, proteinuria, or multi-organ injuries. Mitochondrial-mediated placental oxidative stress plays a key role in the pathogenesis of PE. However, the underlying mechanism remains to be revealed. Here, we identify Rnd3, a small Rho GTPase, regulating placental mitochondrial reactive oxygen species (ROS). We showed that Rnd3 is down-regulated in primary trophoblasts isolated from PE patients. Loss of Rnd3 in trophoblasts resulted in excessive ROS generation, cell apoptosis, mitochondrial injury, and proton leakage from the respiratory chain. Moreover, Rnd3 overexpression partially rescues the mitochondrial defects and oxidative stress in human PE primary trophoblasts. Rnd3 physically interacts with the peroxisome proliferators-activated receptor γ (PPARγ) and promotes the PPARγ-mitochondrial uncoupling protein 2 (UCP2) cascade. Forced expression of PPARγ rescues deficiency of Rnd3-mediated mitochondrial dysfunction. We conclude that Rnd3 acts as a novel protective factor in placental mitochondria through PPARγ-UCP2 signaling and highlight that downregulation of Rnd3 is a potential factor involved in PE pathogenesis.
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http://dx.doi.org/10.1096/fj.202002639RRRDOI Listing
June 2021

Similar Antimicrobial Resistance of Strains Isolated from Retail Chickens and Poultry Farms.

Foodborne Pathog Dis 2021 07 25;18(7):489-496. Epub 2021 May 25.

Institute of Agro-Product Safety and Nutrition, State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-Products, Zhejiang Academy of Agricultural Sciences, Hangzhou, China.

Antimicrobial resistance (AMR) is a major public health challenge and spreads through humans, animals, and the environment. Many reports show that AMR genes (ARGs) or phenotypes can be transferred from food animals to humans. However, the level and correlation of AMR in different nodes of the poultry meat supply chain are still poorly understood. Herein, 225 isolates were recovered from chilled chicken samples from markets (123) and chicken fecal samples from farms (102) in Zhejiang Province, China. The dominant sequence types (STs) were ST155 (8.89%), ST48 (7.56%), and ST10 (7.11%), which are common in chicken and fecal samples. Antimicrobial susceptibility testing (AST) analysis showed that the isolates from fecal samples and retail chickens were resistant to ampicillin (61.77% and 63.42%, respectively) and trimethoprim (56.87% and 52.85%). Moreover, 36.59% of the isolates from chilled chickens and 39.22% of the isolates from fecal samples were resistant to three or more antimicrobial agents. A total of 59 ARGs were identified in sequenced genomes, including the gene involved in colistin resistance. The from farms and markets could be clustered in the same branch according to core single nucleotide polymorphisms. In addition, toxin genes and were also predicted in 86.5% (32/37) and 13.5% (5/37) of the above genomes, respectively. Taken together, these findings demonstrated that isolates from markets and farms showed similar AMR patterns, suggesting that strains in markets may originate from farms.
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http://dx.doi.org/10.1089/fpd.2021.0019DOI Listing
July 2021
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