Publications by authors named "Jinghao Wang"

25 Publications

  • Page 1 of 1

Clinical Evidence of Tai Chi Exercise Prescriptions: A Systematic Review.

Evid Based Complement Alternat Med 2021 10;2021:5558805. Epub 2021 Mar 10.

School of Physical Education & Sports Science, South China Normal University, Guangzhou 510006, China.

Objectives: This systematic review aims to summarize the existing literature on Tai Chi randomized controlled trials (RCTs) and recommend Tai Chi exercise prescriptions for different diseases and populations.

Methods: A systematic search for Tai Chi RCTs was conducted in five electronic databases (PubMed, Cochrane Library, EMBASE, EBSCO, and Web of Science) from their inception to December 2019. SPSS 20.0 software and Microsoft Excel 2019 were used to analyze the data, and the risk of bias tool in the RevMan 5.3.5 software was used to evaluate the methodological quality of RCTs.

Results: A total of 139 articles were identified, including diseased populations (95, 68.3%) and healthy populations (44, 31.7%). The diseased populations included the following 10 disease types: musculoskeletal system or connective tissue diseases (34.7%), circulatory system diseases (23.2%), mental and behavioral disorders (12.6%), nervous system diseases (11.6%), respiratory system diseases (6.3%), endocrine, nutritional or metabolic diseases (5.3%), neoplasms (3.2%), injury, poisoning and certain other consequences of external causes (1.1%), genitourinary system diseases (1.1%), and diseases of the eye and adnexa (1.1%). Tai Chi exercise prescription was generally classified as moderate intensity. The most commonly applied Tai Chi style was Yang style (92, 66.2%), and the most frequently specified Tai Chi form was simplified 24-form Tai Chi (43, 30.9%). 12 weeks and 24 weeks, 2-3 times a week, and 60 min each time was the most commonly used cycle, frequency, and time of exercise in Tai Chi exercise prescriptions.

Conclusions: We recommend the more commonly used Tai Chi exercise prescriptions for different diseases and populations based on clinical evidence of Tai Chi. Further clinical research on Tai Chi should be combined with principles of exercise prescription to conduct large-sample epidemiological studies and long-term prospective follow-up studies to provide more substantive clinical evidence for Tai Chi exercise prescriptions.
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http://dx.doi.org/10.1155/2021/5558805DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7972853PMC
March 2021

Accelerating H2 Evolution by Anodic Semi-dehydrogenation of Tetrahydroisoquinolines in Water over Co3O4 Nanoribbon Arrays Decorated Nickel Foam.

Chemistry 2021 Mar 26. Epub 2021 Mar 26.

Jianghan University, Key Laboratory of Optoelectronic Chemical Materials and Devices of Ministry of Education, Key Laboratory of Optoelectronic Chemical Materials and Devices of Ministry of E, 430056, Wuhan, CHINA.

Coupling H 2 evolution reaction in water with thermodynamically favorable organic oxidation reactions is highly desirable, because it can enhance the energy conversion efficiency compared with the electrocatalytic water splitting, and produce value-added chemicals instead of O 2 in anodic reaction. Herein, Co 3 O 4 nanoribbon arrays in situ grown on nickel foam (Co 3 O 4 @NF) was employed as an effective electrocatalyst for the selective oxidation of tetrahydroisoquinolines (THIQs). Various value-added semi-dehydrogenation products including dihydroisoquinolines with electro-deficient or rich groups could be obtained with moderate yields and faradaic efficiencies. Benefitting from the rich surface active sites of Co 3 O 4 @NF, a two-electrode (Co 3 O 4 @NF || Pt) electrolytic system drove a benchmark current density of 10 mA cm -2 at a cell voltage as low as 1.446 V in 1.0 M KOH aqueous solution containing 0.02 M THIQ, which was reduced by 174 mV in comparison with that of overall water splitting.
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http://dx.doi.org/10.1002/chem.202100249DOI Listing
March 2021

Recent developments on PET radiotracers for TSPO and their applications in neuroimaging.

Acta Pharm Sin B 2021 Feb 25;11(2):373-393. Epub 2020 Aug 25.

Division of Nuclear Medicine and Molecular Imaging, Massachusetts General Hospital & Department of Radiology, Harvard Medical School, Boston, MA 02114, USA.

The 18 kDa translocator protein (TSPO), previously known as the peripheral benzodiazepine receptor, is predominately localized to the outer mitochondrial membrane in steroidogenic cells. Brain TSPO expression is relatively low under physiological conditions, but is upregulated in response to glial cell activation. As the primary index of neuroinflammation, TSPO is implicated in the pathogenesis and progression of numerous neuropsychiatric disorders and neurodegenerative diseases, including Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), multiple sclerosis (MS), major depressive disorder (MDD) and obsessive compulsive disorder (OCD). In this context, numerous TSPO-targeted positron emission tomography (PET) tracers have been developed. Among them, several radioligands have advanced to clinical research studies. In this review, we will overview the recent development of TSPO PET tracers, focusing on the radioligand design, radioisotope labeling, pharmacokinetics, and PET imaging evaluation. Additionally, we will consider current limitations, as well as translational potential for future application of TSPO radiopharmaceuticals. This review aims to not only present the challenges in current TSPO PET imaging, but to also provide a new perspective on TSPO targeted PET tracer discovery efforts. Addressing these challenges will facilitate the translation of TSPO in clinical studies of neuroinflammation associated with central nervous system diseases.
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http://dx.doi.org/10.1016/j.apsb.2020.08.006DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7893127PMC
February 2021

MicroRNA-369 attenuates hypoxia-induced cardiomyocyte apoptosis and inflammation via targeting TRPV3.

Braz J Med Biol Res 2021 15;54(3):e10550. Epub 2021 Jan 15.

Department of Pharmacology, Harbin Medical University-Daqing, Daqing, China.

Hypoxia-induced apoptosis and inflammation play an important role in cardiovascular diseases including myocardial infarction (MI). miR-369 has been suggested to be a key regulator of cardiac fibrosis. However, the role of miR-369 in regulating hypoxia-induced heart injury remains unknown. Our data indicated that miR-369 expression was significantly down-regulated and TRPV3 was significantly up-regulated in myocardial tissue after MI in rats and in hypoxic-treated neonatal rat cardiomyocytes (NRCMs). In addition, we observed that hypoxia significantly promoted apoptosis and the inflammatory response, accompanied by increased caspase-3 activity and the secretion of the cytokines interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α. miR-369 overexpression significantly suppressed cell apoptosis and inflammatory factor production triggered by hypoxia, whereas miR-369 inhibition had an opposite effect. Importantly, we identified TRPV3 as a direct target of miR-369-3p. TRPV3 inhibition with small interfering RNA (siRNA) significantly inhibited hypoxia-induced inflammation and apoptosis, which can reverse the injury effects of miR-369 inhibitors. Our findings indicated that miR-369 reduced hypoxia-induced apoptosis and inflammation by targeting TRPV3.
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http://dx.doi.org/10.1590/1414-431X202010550DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7812908PMC
January 2021

Molybdenum contamination dispersion from mining site to a reservoir.

Ecotoxicol Environ Saf 2021 Jan 13;208:111631. Epub 2020 Nov 13.

School of Environmental and Municipal Engineering, North China University of Water Resources and Electric Power, Zhengzhou 450011, China.

This study was conducted to assess heavy metals in the overlying water and sediments of Luhun Reservoir, Henan Province, China, which is positioned downstream from a molybdenum (Mo) mining area. The pollution indexes indicated that deposition of all metals may have been affected by the mining area. The single element pollution factor (P) of Mo was the highest among all heavy metals, with a mean value of 2.05. However, the sediments were subject to long-term accumulation of metals, particularly Mo, Cd, Pb, and Zn, which originated from anthropogenic sources. The mean individual element potential ecological risk index values for Cd were above 385, while the mean value comprehensive potential ecological risk index was 465, which indicates a high ecological risk. Moreover, the enriched heavy metals had different spatial distributions in the Luhun Reservoir sediments. Finally, Pearson correlation analysis indicated that the Pb was mainly affected by different anthropogenic sources and had no relationship with other metals, which suggests that the influence of mining area on heavy metal concentrations in the reservoir is difficult to disentangle.
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http://dx.doi.org/10.1016/j.ecoenv.2020.111631DOI Listing
January 2021

Neuropeptide Y mediates cardiac hypertrophy through microRNA-216b/FoxO4 signaling pathway.

Int J Med Sci 2021 1;18(1):18-28. Epub 2021 Jan 1.

Department of Pharmacology, Harbin Medical University-Daqing, Daqing, Heilongjiang 163319, China.

Cardiac hypertrophy (CH) is a major risk factor for heart failure accompanied by maladaptive cardiac remodeling. The role and potential mechanism of neuropeptide Y (NPY) in CH are still unclear. We will explore the role and the mechanism of NPY inactivation (NPY-I) in CH caused by pressure overload. Abdominal aortic constriction (AAC) was used to induce CH model in rats. NPY or angiotensin II (Ang II) was used to trigger CH model in neonatal rat ventricular myocytes (NRVMs). We found that NPY was increased in the heart and plasma of hypertrophic rats. However, Ang II did not increase NPY expression in cardiomyocytes. NPY-I attenuated CH as decreasing CH-related markers (ANP, BNP and β-MHC mRNA) level, reducing cell surface area, and restoring cardiac function. NPY inactivation increased miR-216b and decreased FoxO4 expression in CH heart. Moreover, NPY decreased miR-216b and increased FoxO4 expression in NRVMs which were reversed by NPY type 1 receptor (NPY1R) antagonist BIBO3304. MiR-216b mimic and FoxO4 siRNA (small interfering RNA) inhibited NPY/Ang II-induced myocardial hypertrophy . Meanwhile, BIBO3304 reversed the pro-hypertrophy effect of NPY . Collectively, NPY deficiency attenuated CH by NPY1R-miR-216b-FoxO4 axis. These findings suggested that NPY would be a potential therapeutic target for the prevention and treatment of cardiac hypertrophy.
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http://dx.doi.org/10.7150/ijms.51133DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7738963PMC
January 2021

Creating the position of surgical pharmacist in China.

Eur J Hosp Pharm 2020 11 27;27(6):e99. Epub 2020 Feb 27.

Guangdong Province Pharmaceutical Association, Guangzhou, China.

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http://dx.doi.org/10.1136/ejhpharm-2020-002238DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7856123PMC
November 2020

Elevated DHODH expression promotes cell proliferation via stabilizing β-catenin in esophageal squamous cell carcinoma.

Cell Death Dis 2020 10 15;11(10):862. Epub 2020 Oct 15.

Cancer Institute, Peking University Shenzhen Hospital, Shenzhen Peking University-Hong Kong University of Science and Technology (PKU-HKUST) Medical Center, 518035, Shenzhen, People's Republic of China.

As a key enzyme in de novo pyrimidine biosynthesis, the expression level of dihydroorotate dehydrogenase (DHODH) has been reported to be elevated in various types of malignant tumors and its tumor-promoting effect was considered to relate to its pyrimidine synthesis function. Here, we revealed one intriguing potential mechanism that DHODH modulated β-catenin signaling in esophageal squamous cell carcinoma (ESCC). We demonstrated that DHODH directly bound to the NH2 terminal of β-catenin, thereby, interrupting the interaction of GSK3β with β-catenin and leading to the abrogation of β-catenin degradation and accumulation of β-catenin in the nucleus, which in turn, resulted in the activation of β-catenin downstream genes, including CCND1, E2F3, Nanog, and OCT4. We further demonstrated that the regulation of β-catenin by DHODH was independent of DHODH catalyzing activity. Univariate and multivariate analyses suggested that DHODH expression might be an independent prognostic factor for ESCC patients. Collectively, our study highlights the pivotal role of DHODH mediated β-catenin signaling and indicates that DHODH may act as a multi-functional switcher from catalyzing pyrimidine metabolism to regulating tumor-related signaling pathways in ESCC.
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http://dx.doi.org/10.1038/s41419-020-03044-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7566478PMC
October 2020

Electron transfer involved in bio-Pd (0) synthesis by Citrobacter freundii at different growth phases.

Ecotoxicol Environ Saf 2020 Mar 26;190:110124. Epub 2019 Dec 26.

Ministry of Education Key Laboratory of Pollution Control and Ecological Remediation for Industrial Agglomeration Area, School of Environment and Energy, South China University of Technology, Guangzhou, 510006, China.

Gram-negative Citrobacter freundii with high Pd (II) reduction capacity was isolated from electroplating wastewater, and the electron transfer involved in Pd (II) bio-reduction by C. freundii JH was investigated in phosphate buffer saline solution with sodium formate as sole electron donor under anaerobic condition. FTIR spectra indicated that hydroxyl and amine groups on cell wall participated Pd (II) bio-sorption. TEM, XRD, XPS results confirmed that Pd (0) nanoparticles (NPs) could be bio-synthesized intra/extracellularly. Meanwhile, pH turn-over were observed owing to the reduction of cytochrome c (c-Cyt) in bio-reduction process. EPR spectra indicated that free radicals (OH) was generated from high concentration Pd (II), which would cause seriously damage to cell. Despite of the lower tolerance to Pd (II), the cells at logarithmic phase exhibited higher Pd (II) reduction capacity (72.21%) than that at stationary phase (56.21%), which might be related to the relatively stronger proton motive force (PMF) created by the substrate oxidation and the electron transfer, as evidenced by electrochemical experiments (CV, DPV, amperometric I-t curves) and protein denaturalization experiments. Additionally, c-Cyt and riboflavin were confirmed to be important participants in electron transfer. Finally, a putative synthesis mechanism of Pd (0)-NPs was deduced. This study contributed to further understanding the electron transfer in Pd (II) reduction, and provided more information for the bio-synthetic of metal nanoparticles.
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http://dx.doi.org/10.1016/j.ecoenv.2019.110124DOI Listing
March 2020

Novel lncRNA PSMG3‑AS1 functions as a miR‑143‑3p sponge to increase the proliferation and migration of breast cancer cells.

Oncol Rep 2020 Jan 25;43(1):229-239. Epub 2019 Oct 25.

Central Laboratory of The Fifth Affiliated Hospital of Harbin Medical University, Daqing, Heilongjiang 163711, P.R. China.

Long non‑coding RNAs (lncRNAs) are considered to be important regulators in breast cancer. In the present study, the potential mechanisms and functional roles of lncRNA PSMG3‑antisense (AS)1 were investigated in vivo and in vitro. The relative expression levels of lncRNA PSMG3‑AS1 and microRNA (miR)‑143‑3p were determined using reverse‑transcription quantitative PCR. The protein expression levels of collagen type 1 alpha 1 (COL1A1) and proliferating cell nuclear antigen (PCNA) were obtained using western blot analysis. Bioinformatics analysis was used to identify the relationship between PSMG3‑AS1, miR‑143‑3p and COL1A1. Colony forming and Cell Counting Kit‑8 assays were used to detect cell proliferation. Transwell and wound‑healing assays were used to determine cell migration. The results of the present study demonstrated that PSMG3‑AS1 expression was increased in breast cancer tumor tissues and cell lines, and that of miR‑143‑3p was decreased. Knockdown of PSMG3‑AS1 increased the level of miR‑143‑3p expression, which led to the mitigation of proliferation and migration capacity in breast carcinoma cells. Additionally, PSMG3‑AS1 knockdown was demonstrated to reduce the mRNA and protein expression levels of COL1A1. miR‑143‑3p mimic transfection reduced proliferation and migration in MDA‑MB‑231 and MCF‑7 cell lines. Furthermore, miR‑143‑3p inhibition significantly increased the proliferation and migration of breast cancer cells compared with the negative control group. The mRNA and protein expression levels of PCNA were reduced in the MCF‑7 cell line when transfected with miR‑143‑3p mimics and si‑PSMG3‑AS1. However, PCNA expression was increased in cells transfected with a miR‑143‑3p inhibitor. In conclusion, the results of the present study identified a novel lncRNA PSMG3‑AS1, which serves as a sponge for miR‑143‑3p in the pathogenesis of breast cancer. PSMG3‑AS1 may be used as a potential therapeutic target gene in breast cancer treatment.
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http://dx.doi.org/10.3892/or.2019.7390DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6908943PMC
January 2020

Surface-emitting distributed feedback laser based on high-order gratings.

Appl Opt 2019 Jul;58(20):5443-5449

This paper reports a surface-emitting (SE) distributed feedback laser based on high-order surface gratings. The proposed device not only retains the advantages of edge-emitting lasers such as excellent single-mode property, high internal quantum efficiency, and high output power but also obtains other appealing characteristics, such as easy realization of the hybrid integration, the simple fabrication process, etc. The SE distributed feedback laser is analyzed and optimized for better performances using an improved traveling wave model.
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http://dx.doi.org/10.1364/AO.58.005443DOI Listing
July 2019

SHCBP1 regulates apoptosis in lung cancer cells through phosphatase and tensin homolog.

Oncol Lett 2019 Aug 24;18(2):1888-1894. Epub 2019 Jun 24.

Department of Pharmacy, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong 510630, P.R. China.

Src homologous and collagen (SHC) SH2-binding protein 1 (SHCBP1) is a member of the SHC family, and is overexpressed in numerous types of cancer. In addition, apoptosis serves an important role in the development of cancer. The purpose of this study was to examine the effect of SHCBP1 on apoptosis and its potential underlying mechanism in lung cancer cells. Apoptosis was detected by flow cytometry and caspase-3 activity analysis. The expression levels of SHCBP1 and phosphatase and tensin homolog (PTEN) were detected by western blot analysis and reverse transcription-quantitative polymerase chain reaction. Cell viability was determined by MTT assay. The results indicated that SHCBP1 was increased in lung cancer cell lines and lung cancer tissues compared with in normal lung cell lines and tissues. The apoptosis of lung cancer cells was significantly increased by SHCBP1 small interfering RNA (siRNA), as indicated by the increased number of apoptotic cells and enhanced caspase-3 activity. In addition, it was demonstrated that PTEN expression was modulated by SHCBP1 knockdown; silencing of SHCBP1 expression led to a significant increase in PTEN expression. Furthermore, inhibition of PTEN by siRNA reversed the increase in apoptosis induced by SHCBP1 siRNA. These results suggested that SHCBP1 may be upregulated in lung cancer and it may serve a key role in the apoptosis of lung cancer cells; this effect was associated with the expression of PTEN.
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http://dx.doi.org/10.3892/ol.2019.10520DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6614682PMC
August 2019

Spread of the idea of 'deprescribing' in China.

Eur J Hosp Pharm 2019 Jul 20;26(4):241-242. Epub 2019 Mar 20.

Department of Pharmacy, Jinan University First Affiliated Hospital, Guangzhou, China.

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http://dx.doi.org/10.1136/ejhpharm-2019-001907DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6613922PMC
July 2019

miR-216a promotes breast cancer cell apoptosis by targeting PKCα.

Fundam Clin Pharmacol 2019 Aug 31;33(4):397-404. Epub 2019 May 31.

Department of Medical Oncology, Harbin Medical University Cancer Hospital, Heilongjiang, 150081, China.

Breast cancer (BC) is the most common cause of death in women throughout the world. MicroRNAs (miRNAs, miR) have been identified as key regulators in carcinogenesis of several cancers, including BC. MicroRNA-216a (miR-216a) is downregulated in several cancers. Here, we evaluated the effects of miRNA-216a on breast cancer cells and the underlying mechanisms. miR-216a level was quantified by real-time RT-PCR. Cell viability was analyzed by MTT assay. Wound-healing assay was performed for detection of cell migration. Apoptosis was detected by TUNEL and caspase-3 activity assay. Moreover, the level of protein expression was determined by Western blot. We found that miR-216a expression was remarkably decreased in both human BC tissues and MCF-7 cells. miR-216a overexpression dramatically suppressed the migration and promoted the apoptosis in cultured MCF-7 cells. We validated PKCα (protein kinase C alpha, PRKCA) as a direct target of miR-216a. Knockdown of PKCα induced apoptosis and inhibited migration in cultured MCF-7 cells which were reversed by miR-216a inhibitor. Moreover, the level of miR-216a is negatively correlated with PKCα in cell lines. Our results collectively suggest that miR-216a suppressed migration and promoted apoptosis in breast cancer cells by targeting PKCα. These findings indicate that manipulation of miR-216a expression may represent a novel therapeutic strategy in the treatment of breast cancer.
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http://dx.doi.org/10.1111/fcp.12481DOI Listing
August 2019

Overexpression of PDK4 is associated with cell proliferation, drug resistance and poor prognosis in ovarian cancer.

Cancer Manag Res 2019 24;11:251-262. Epub 2018 Dec 24.

Department of Biotherapy, Shanxi Provincial Cancer Hospital, Taiyuan, Shanxi 030013, China,

Purpose: Ovarian cancer is a major type of gynecological malignancy which characterized by the chemoresistance, heterogeneity and highly metastasis. However, the mechanism underlying the progression of ovarian cancer remains elusive. Pyruvate dehydrogenase kinase family plays critical roles in tumorigenesis, and PDK4 has been demonstrated to be an oncogene in many types of cancers. The aim of this study was to identify the role of PDK4 in ovarian cancer.

Methods: We explored the PDK4 expression according to the public database containing patients with different effect of chemotherapy. Cell proliferation and invasion assays were used to determine the function of PDK4. Mice xenograft experiment was conducted to test the pro-tumorigenesis function of PDK4 in vivo. Cell apoptosis under treatment of chemo drugs was detected by flow cytometry and TUNEL analysis. Spheroid formation assay and CD133+ cell population were used to determine the PDK4-induced stem-like traits. Immunohistochemical staining was performed to test the expression of PDK4 in ovarian cancer tissues, and Kaplan- Meier curve with log-rank test was performed to determine the association between PDK4 expression and ovarian cancer patients' prognosis.

Results: Overexpression of PDK4 markedly promoted cell proliferation, invasion and tumor growth in vivo. Furthermore, PDK4 confers cell resistant to chemotherapy-induced apoptosis. Mechanically, we demonstrated that PDK4 induced stem-like traits. Meanwhile, PDK4 expression was significantly evaluated in ovarian cancer tissues compared to that in adjacent non-cancer tissues, and high expression of PDK4 was associated with poor overall survival and progression-free survival of ovarian cancer patients.

Conclusion: These results identify a novel role of PDK4 in regulating cell stem-like trait, which directly enhances the cell proliferation, invasion and chemoresistance in ovarian cancer, and targeting PDK4 could be a potential approach for ovarian cancer treatments.
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http://dx.doi.org/10.2147/CMAR.S185015DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6307676PMC
December 2018

JARID1B modulates breast cancer cell apoptosis by regulating p53 expression.

Int J Clin Exp Pathol 2018 1;11(9):4529-4536. Epub 2018 Sep 1.

Institute of New Drug Research and Guangzhou Key Laboratory of Innovative Chemical Drug Research in Cardio-cerebrovascular Diseases, Jinan University College of Pharmacy Guangzhou, China.

Jumonji AT-rich interactive domain 1B (JARID1B) has been implicated in breast cancer progression, but its role in apoptosis has not been explored. The present study was designed to investigate the effect of JARID1B on breast cancer cell apoptosis. Apoptosis was assessed by TUNEL, flow cytometry and caspase-3 activity. JARID1B and p53 expression were examined by Western blot. Cell viability was measured by an MTT assay. We found that JARID1B is overexpressed in the breast cancer cell line and in breast cancer tissues. Upregulated expression of JARID1B in breast cancer tissues correlates with poor patient prognosis. The apoptosis of breast cancer cells is significantly increased by RNA interference targeting JARID1B. Moreover, the expression of p53 is modulated by JARID1B; the silencing of JARID1B exhibits greatly increased p53 expression at the protein level. The inhibition of p53 by small interfering RNA (siRNA) reverses the JARID1B siRNA-induced increase of apoptosis. Our results collectively suggest that JARID1B plays a key role in breast cancer cell apoptosis, and it may partially achieve this role through p53.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6962977PMC
September 2018

High efficiency all-fiber cylindrical vector beam laser using a long-period fiber grating.

Opt Lett 2018 Feb;43(4):755-758

We demonstrate a novel all-fiber laser generating cylindrical vector beams with high slope efficiency and low threshold by introducing a long-period fiber grating into the laser cavity. Highly efficient mode conversion is realized by an LPFG at ∼1548  nm. Mode selection and spectrum filtering are achieved in combination with a two-mode fiber Bragg grating (TM-FBG). The fiber laser operates at a single wavelength of 1547.95 nm with a 30 dB linewidth of less than 0.18 nm and a side-mode suppression ratio (SMSR) of more than 56 dB. The lasing threshold and slope efficiency of the laser are 24.5 mW and 35.41%, respectively. The output power is 72 mW with an absorbed pump power of 225 mW. The variation of slope efficiency with respect to the reflectivity of the TM-FBG is investigated. Through adjusting the intra-cavity polarization controller, high-purity radially and azimuthally polarized beams are both obtained.
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http://dx.doi.org/10.1364/OL.43.000755DOI Listing
February 2018

[IL-1β promotes the proliferation of astrocytes and downregulates the expression of Kir4.1].

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2017 Apr;33(4):446-449

Anhui Clinical and Preclinical Key Laboratory of Respiratory Disease, First Affiliated Hospital, Bengbu Medical College, Bengbu 233030, China. *Corresponding author, E-mail:

Objective To explore the impact of IL-1β on the proliferation of astrocytes and the expression of the inwardly rectifying potassium channel 4.1 (Kir4.1) in astrocytes. Methods Astrocytes were isolated from cerebral cortex of newborn SD rats and cultured in the presence of IL-1β or IL-1β combined with interleukin-1 receptor antagonist (IL-1Ra). The effect of IL-1β on the cell cycle of astrocytes was measured with flow cytometry; the level of Kir4.1 mRNA was determined by quantitative real-time PCR. The level of Kir4.1 protein was detected by Western blotting. Results IL-1β promoted astrocyte proliferation in a time- and dose-dependent manner. After astrocytes were treated with IL-1β (10 ng/mL) for 24 hours, the levels of Kir4.1 mRNA and protein significantly decreased, but IL-1Ra significantly inhibited IL-1β-induced decrease of Kir4.1. The downregulation of Kir4.1 mRNA and protein expressions could be partially reverted when IL-1β was removed. Conclusion IL-1β could promote the proliferation of cultured astrocytes, and IL-1β may be a key factor influencing the expression of Kir4.1 in astrocytes.
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April 2017

LTPB2 acts as a prognostic factor and promotes progression of cervical adenocarcinoma.

Am J Transl Res 2015 15;7(6):1095-105. Epub 2015 Jun 15.

Obstetrics and Gynecology Hospital, Fudan University Shanghai 200011, PR China ; Department of Obstetrics and Gynecology of Shanghai Medical College, Fudan University Shanghai 200032, PR China ; Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases Shanghai 200011, PR China ; Cancer Institute, Fudan University Shanghai Cancer Center Shanghai 200032, PR China ; Institutes of Biomedical Sciences, Fudan University Shanghai 200032, PR China.

Latent transforming growth factor-beta-1 binding protein-2 (LTBP-2) is a member of the fibrillin/LTBP super family of extracellular matrix proteins, found to be overexpressed in certain malignant tumors. However, the clinical significance and biological role of LTBP-2 in cervical adenocarcinoma has remains unclear. We found that the expression of LTBP2 was higher in cervical adenocarcinoma than in normal cervical epithelial tissue as assessed by immunohistochemistry. Expression of LTBP2 is related to clinical stage, cervical tumor size, depth of cervical stromal invasion and lymph node metastasis. Knockdown of LTBP2 expression can inhibit the proliferation and migration of HeLa cells. Moreover, LTBP2 knockdown affected multiple tumor-related pathway genes including: the MAPK signaling pathway, the PI3K-AKT signaling pathway, receptor tyrosine kinase signaling and the P53 pathway. Taken together, this work suggests that LTBP2 may promote the development of cervical adenocarcinoma and serve as a prognostic factor in the clinical evaluation of patients with cervical adenocarcinoma. Our findings provide a new strategy for the diagnosis and treatment of cervical adenocarcinoma.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4532742PMC
August 2015

Suppression of AKT expression by miR-153 produced anti-tumor activity in lung cancer.

Int J Cancer 2015 Mar 7;136(6):1333-40. Epub 2014 Aug 7.

Department of Pharmacology, Key Laboratory of Cardiovascular Medicine Research, Ministry of Education; State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.

Lung cancer is one of the leading causes of cancer death worldwide. microRNAs have been shown to be a novel class of regulators in lung cancer. Here, we explored the role of miR-153 in the pathogenesis of lung cancer and its therapeutic potential. miR-153 was significantly decreased in lung cancer tissues than the adjacent tissues. The protein and mRNA levels of protein kinase B (AKT), which were shown to promote tumor growth, were both increased in lung cancer tissues than adjacent tissues. Overexpression of miR-153 significantly inhibited AKT protein expression, which were abrogated by co-transfection of AMO-153, the specific inhibitor of miR-153. Luciferase assay showed that transfection of miR-153 markedly suppressed the fluorescent intensity of chimeric vectors carrying the 3'UTR of AKT1, while produced no effect on the mutant construct, indicating that AKT is regulated by miR-153. Overexpression of miR-153 significantly inhibited the proliferation and migration, and promoted apoptosis of cultured lung cancer cells in vitro, and suppressed the growth of xenograft tumors in vivo. Interestingly, lung cancer cells with lower endogenous miR-153 expression are more sensitive to ectopic overexpressed miR-153. The IC50 of miR-153 on lung cancer cells is positive correlated with the endogenous miR-153 level, while negative correlated with AKT level. Knockdown of AKT expression suppressed lung cancer cell proliferation. In summary, miR-153 exerted anti-tumor activity in lung cancer by targeting on AKT. The sensitivity of lung cancer cells to miR-153 is determined by its endogenous miR-153 level.
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http://dx.doi.org/10.1002/ijc.29103DOI Listing
March 2015

miR-1 exacerbates cardiac ischemia-reperfusion injury in mouse models.

PLoS One 2012 30;7(11):e50515. Epub 2012 Nov 30.

Department of Pharmacology-Key Laboratory of Cardiovascular Medicine Research, Ministry of Education, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.

Recent studies have revealed the critical role of microRNAs (miRNAs) in regulating cardiac injury. Among them, the cardiac enriched microRNA-1(miR-1) has been extensively investigated and proven to be detrimental to cardiac myocytes. However, solid in vivo evidence for the role of miR-1 in cardiac injury is still missing and the potential therapeutic advantages of systemic knockdown of miR-1 expression remained unexplored. In this study, miR-1 transgenic (miR-1 Tg) mice and locked nucleic acid modified oligonucleotide against miR-1 (LNA-antimiR-1) were used to explore the effects of miR-1 on cardiac ischemia/reperfusion injury (30 min ischemia followed by 24 h reperfusion). The cardiac miR-1 level was significantly increased in miR-1 Tg mice, and suppressed in LNA-antimiR-1 treated mice. When subjected to ischemia/reperfusion injury, miR-1 overexpression exacerbated cardiac injury, manifested by increased LDH, CK levels, caspase-3 expression, apoptosis and cardiac infarct area. On the contrary, LNA-antimiR-1 treatment significantly attenuated cardiac ischemia/reperfusion injury. The expression of PKCε and HSP60 was significantly repressed by miR-1 and enhanced by miR-1 knockdown, which may be a molecular mechanism for the role miR-1 in cardiac injury. Moreover, luciferase assay confirmed the direct regulation of miR-1 on protein kinase C epsilon (PKCε) and heat shock protein 60 (HSP60). In summary, this study demonstrated that miR-1 is a causal factor for cardiac injury and systemic LNA-antimiR-1 therapy is effective in ameliorating the problem.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0050515PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3511560PMC
May 2013

MicroRNA-101 inhibited postinfarct cardiac fibrosis and improved left ventricular compliance via the FBJ osteosarcoma oncogene/transforming growth factor-β1 pathway.

Circulation 2012 Aug 18;126(7):840-50. Epub 2012 Jul 18.

Department of Pharmacology (the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), Harbin Medical University, Harbin, China.

Background: Cardiac interstitial fibrosis is a major cause of the deteriorated performance of the heart in patients with chronic myocardial infarction. MicroRNAs (miRs) have recently been proven to be a novel class of regulators of cardiovascular diseases, including those associated with cardiac fibrosis. This study aimed to explore the role of miR-101 in cardiac fibrosis and the underlying mechanisms.

Methods And Results: Four weeks after coronary artery ligation of rats, the expression of miR-101a and miR-101b (miR-101a/b) in the peri-infarct area was decreased. Treatment of cultured rat neonatal cardiac fibroblasts with angiotensin II also suppressed the expression of miR-101a/b. Forced expression of miR-101a/b suppressed the proliferation and collagen production in rat neonatal cardiac fibroblasts, as revealed by cell counting, MTT assay, and quantitative reverse transcription-polymerase chain reaction. The effect was abrogated by cotransfection with AMO-101a/b, the antisense inhibitors of miR-101a/b. c-Fos was found to be a target of miR-101a because overexpression of miR-101a decreased the protein and mRNA levels of c-Fos and its downstream protein transforming growth factor-β1. Silencing c-Fos by siRNA mimicked the antifibrotic action of miR-101a, whereas forced expression of c-Fos protein canceled the effect of miR-101a in cultured cardiac fibroblasts. Strikingly, echocardiography and hemodynamic measurements indicated remarkable improvement of the cardiac performance 4 weeks after adenovirus-mediated overexpression of miR-101a in rats with chronic myocardial infarction. Furthermore, the interstitial fibrosis was alleviated and the expression of c-Fos and transforming growth factor-β1 was inhibited.

Conclusion: Overexpression of miR-101a can mitigate interstitial fibrosis and the deterioration of cardiac performance in postinfarct rats, indicating the therapeutic potential of miR-101a for cardiac disease associated with fibrosis.
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http://dx.doi.org/10.1161/CIRCULATIONAHA.112.094524DOI Listing
August 2012

microRNA-124 regulates cardiomyocyte differentiation of bone marrow-derived mesenchymal stem cells via targeting STAT3 signaling.

Stem Cells 2012 Aug;30(8):1746-55

Department of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education, Harbin, Heilongjiang Province, China.

Accumulating evidence demonstrated that bone marrow-derived mesenchymal stem cells (BMSCs) may transdifferentiate into cardiomyocytes and replace apoptotic myocardium so as to improve functions of damaged hearts. However, little information is known about molecular mechanisms underlying myogenic conversion of BMSCs. microRNAs as endogenous noncoding small molecules function to inhibit protein translation post-transcriptionally by binding to complementary sequences of targeted mRNAs. Here, we reported that miR-124 was remarkably downregulated during cardiomyocyte differentiation of BMSCs induced by coculture with cardiomyocytes. Forced expression of miR-124 led to a significant downregulation of cardiac-specific markers-ANP, TNT, and α-MHC proteins as well as reduction of cardiac potassium channel currents in cocultured BMSCs. On the contrary, the inhibition of endogenous miR-124 with its antisense oligonucleotide AMO-124 obviously reversed the changes of ANP, TNT, and α-MHC proteins and increased cardiac potassium channel currents. Further study revealed that miR-124 targeted the 3'UTR of STAT3 gene so as to suppress the expression of STAT3 protein but did not affect its mRNA level. STAT3 inhibitors AG490, WP1066, and S3I-201 were shown to attenuate the augmented expression of ANP, TNT, α-MHC, GATA-4 proteins, and mRNAs in cocultured BMSCs with AMO-124 transfection. Moreover, GATA-4 siRNA reduced the expression of ANP, TNT, α-MHC, and GATA-4 proteins but did not impact STAT3 protein in cocultured BMSCs, indicating GATA-4 serves as an effector of STAT3. In summary, we found that miR-124 regulated myogenic differentiation of BMSCs via targeting STAT3 mRNA, which provides new insights into molecular mechanisms of cardiomyogenesis of BMSCs.
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http://dx.doi.org/10.1002/stem.1154DOI Listing
August 2012

Scutellarin alleviates interstitial fibrosis and cardiac dysfunction of infarct rats by inhibiting TGFβ1 expression and activation of p38-MAPK and ERK1/2.

Br J Pharmacol 2011 Feb;162(3):688-700

Department of Pharmacology, Harbin Medical University, Harbin, China.

Background And Purpose: Interstitial fibrosis plays a causal role in the development of heart failure after chronic myocardial infarction (MI), and anti-fibrotic therapy represents a promising strategy to mitigate this pathological process. The purpose of this study was to investigate the effect of long-term administration of scutellarin (Scu) on cardiac interstitial fibrosis of myocardial infarct rats and the underlying mechanisms.

Experimental Approach: Scu was administered to rats that were subjected to coronary artery ligation. Eight weeks later, its effects on cardiac fibrosis were assessed by examining cardiac function and histology. The number and collagen content of cultured cardiac fibroblasts exposed to angiotensin II (Ang II) were determined after the administration of Scu in vitro. Protein expression was detected by Western blot technique, and mRNA levels by quantitative reverse transcription-PCR.

Key Results: The echocardiographic and haemodynamic measurements showed that Scu improved the impaired cardiac function of infarct rats and decreased interstitial fibrosis. Scu inhibited the expression of FN1 and TGFβ1, but produced no effects on inflammatory cytokines (TNFα, IL-1β and IL-6) in the 8 week infarct hearts. Scu inhibited the proliferation and collagen production of cardiac fibroblasts (CFs) and the up-regulation of FN1 and TGFβ1 induced by Ang II. The enhanced phosphorylation of p38-MAPK and ERK1/2 in both infarct cardiac tissue and cultured CFs challenged by Ang II were suppressed by Scu.

Conclusions And Implications: Long-term administration of Scu improved the cardiac function of MI rats by inhibiting interstitial fibrosis, and the mechanisms may involve the suppression of pro-fibrotic cytokine TGFβ1 expression and inhibition of p38 MAPK and ERK1/2 phosphorylation.
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http://dx.doi.org/10.1111/j.1476-5381.2010.01070.xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3041257PMC
February 2011

Probing the kinetics of short-distance drug release from nanocarriers to nanoacceptors.

Angew Chem Int Ed Engl 2010 Nov;49(45):8426-30

Division of Chemistry and Biological Chemistry, Nanyang Technological University, 21 Nanyang Link, Singapore 637371, Singapore.

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http://dx.doi.org/10.1002/anie.201001065DOI Listing
November 2010