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1,571 results on '"Qian, Zhiyong"'

154. JMJD3 Is Required for Acute Pancreatitis and Pancreatitis-Associated Lung Injury

Author

Chen, Li, primary, Zhang, Xiangxian, additional, Liu, Yu, additional, Liu, Li, additional, Liang, Xiao, additional, Yang, Shengqun, additional, Xia, Qing, additional, Jin, Tao, additional, Ma, Yun, additional, Chen, Yonghua, additional, Yuan, Xia, additional, Tie, Yan, additional, Gu, Yangzhuo, additional, Fang, Chunju, additional, Chen, Siyuan, additional, Mo, Fei, additional, Yu, Ting, additional, Hu, Yuzhu, additional, Qian, Zhiyong, additional, Peng, Yong, additional, Geng, Jia, additional, Zhou, Zongguang, additional, Wu, Min, additional, Ding, Jiansheng, additional, Yang, Daoke, additional, and Wei, Xiawei, additional

Published
2023
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162. Publisher Correction: A vaccine targeting the RBD of the S protein of SARS-CoV-2 induces protective immunity

Author

Yang, Jingyun, Wang, Wei, Chen, Zimin, Lu, Shuaiyao, Yang, Fanli, Bi, Zhenfei, Bao, Linlin, Mo, Fei, Li, Xue, Huang, Yong, Hong, Weiqi, Yang, Yun, Zhao, Yuan, Ye, Fei, Lin, Sheng, Deng, Wei, Chen, Hua, Lei, Hong, Zhang, Ziqi, Luo, Min, Gao, Hong, Zheng, Yue, Gong, Yanqiu, Jiang, Xiaohua, Xu, Yanfeng, Lv, Qi, Li, Dan, Wang, Manni, Li, Fengdi, Wang, Shunyi, Wang, Guanpeng, Yu, Pin, Qu, Yajin, Yang, Li, Deng, Hongxin, Tong, Aiping, Li, Jiong, Wang, Zhenling, Yang, Jinliang, Shen, Guobo, Zhao, Zhiwei, Li, Yuhua, Luo, Jingwen, Liu, Hongqi, Yu, Wenhai, Yang, Mengli, Xu, Jingwen, Wang, Junbin, Li, Haiyan, Wang, Haixuan, Kuang, Dexuan, Lin, Panpan, Hu, Zhengtao, Guo, Wei, Cheng, Wei, He, Yanlin, Song, Xiangrong, Chen, Chong, Xue, Zhihong, Yao, Shaohua, Chen, Lu, Ma, Xuelei, Chen, Siyuan, Gou, Maling, Huang, Weijin, Wang, Youchun, Fan, Changfa, Tian, Zhixin, Shi, Ming, Wang, Fu-Sheng, Dai, Lunzhi, Wu, Min, Li, Gen, Wang, Guangyu, Peng, Yong, Qian, Zhiyong, Huang, Canhua, Lau, Johnson Yiu-Nam, Yang, Zhenglin, Wei, Yuquan, Cen, Xiaobo, Peng, Xiaozhong, Qin, Chuan, Zhang, Kang, Lu, Guangwen, and Wei, Xiawei

Published
2021
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164. Gold Nanorods and Polymer Micelles Mediated Dual TLR Stimulators Delivery System CPG@Au NRs/M‐R848 Regulate Macrophages Reprogramming and DC Maturation for Enhanced Photothermal Immunotherapy of Melanoma

Author

Jia, YanPeng, primary, Shi, Kun, additional, Dai, LiQun, additional, He, XinLong, additional, Deng, HanZhi, additional, Han, RuXia, additional, Yang, Fan, additional, Chu, BingYang, additional, Liao, JinFeng, additional, Wei, XiaWei, additional, and Qian, ZhiYong, additional

Published
2022
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181. CLOCK-BMAL1 regulate the cardiac L-type calcium channel subunit CACNA1C through PI3K-Akt signaling pathway

Author

Chen, Yanhong, Zhu, Didi, Yuan, Jiamin, Han, Zhonglin, Wang, Yao, Qian, Zhiyong, Hou, Xiaofeng, Wu, Tingting, and Zou, Jiangang

Subjects
Arrhythmia -- Physiological aspects, Heart cells -- Physiological aspects, Circadian rhythms -- Physiological aspects, Transcription factors -- Physiological aspects, Biological sciences
Abstract

The heterodimerized transcription factors CLOCK-BMAL1 regulate the cardiomyocyte circadian rhythms. The L-type calcium currents play important role in the cardiac electrogenesis and arrhythmogenesis. Whether and how the CLOCK-BMAL1 regulate the cardiac L-type calcium channels are yet to be determined. The functions of the L-type calcium channels were evaluated with patch clamping techniques. Recombinant adenoviruses of CLOCK and BMAL1 were used in the expression experiments. We reported that the expressions and functions of CACNA1C (the a-subunit of the L-type calcium channels) showed circadian rhythms, with the peak at zeitgeber time 3 (ZT3). The endocardial action potential durations 90 (APD90) were correspondingly longer at ZT3. The protein levels of the phosphorylated Akt at threonine 308 (pAkt T308) also showed circadian rhythms. Overexpressions of CLOCK-BMAL1 significantly reduced the levels of CACNA1C while increasing the levels of pAkt T308 and pik3r1. Furthermore, the inhibitory effects of CLOCK-BMAL1 on CACNA1C could be abolished by the Akt inhibitor MK2206 or the PDK1 inhibitor GSK2334470. Collectively, our findings suggested that the expressions of the cardiac CACNA1C were under the CLOCK-BMAL1 regulation, probably through the PI3K-Akt signal pathway. Key words: L-type calcium currents, cardiomyocyte action potentials, PI3K-Akt pathway, ventricular arrhythmia, circadian rhythm, CLOCK, BMAL1. D'une part, les facteurs de transcription heterodimerises CLOCK et BMAL1 regulent les rythmes circadiens des cardiomyocytes. D'autre part, les courants calciques de type L jouent un role important dans l'electrogenese et l'arythmogenese dans le coeur. Il reste a determiner comment CLOCK et BMAL1 regulent les canaux calciques de type L du coeur. Nous avons evalue le fonctionnement des canaux calciques de type L a l'aide de techniques de patch clamp. Nous avons utilise les adenovirus recombinants de CLOCK et de BMAL1 pour les experiences d'expression. Nous avons observe que l'expression et le fonctionnement de la CACNA1C (la sous-unite a des canaux calciques de type L) presentaient des rythmes circadiens, dont le pic etait au temps zeitgeber 3 (ZT3). En accord avec cela, les durees de potentiel d'action endocardique a 90 % de la repolarisation (APD90) etaient plus importantes a ZT3. Les taux de proteines issues de l'Akt phosphorylee au site threonine 308 (pAkt T308) ont aussi presente des rythmes circadiens. La surexpression de CLOCK et de BMAL1 a entraine une diminution marquee des taux de CACNA1C ainsi qu'une augmentation des taux de pAkt T308 et de pik3r1. De surcroit, les effets inhibiteurs de CLOCK et de BMAL1 sur la CACNA1C pouvaient etre supprimes par le MK2206, un inhibiteur de l'Akt, ou le GSK2334470, un inhibiteur de la PDK1. Dans l'ensemble, nos resultats laissent entendre que les expressions de la CACNA1C cardiaque subiraient la regulation de CLOCK et de BMAL1, probablement par l'intermediaire de la voie de signalisation PI3K-Akt. [Traduit par la Redaction] Mots-cles: courants calciques de type L, potentiels d'action de cardiomyocytes, voie de signalization PI3K-Akt, arythmie ventriculaire, rythme circadian, CLOCK, BMAL1., Introduction The incidence of ventricular arrhythmias (VA) and sudden cardiac death (SCD) exhibit diurnal rhythms, with the well-known morning peaks (Arntz et al. 1993; Muller et al. 1987; Willich et [...]

Published
2016
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197. Clinical Significance of HSCARG for Atherosclerotic Coronary Heart Disease and Reduced ROS-Oxidative Stress in in Vivo and in Vitro Models via p47phox by NF-κB Activity

Author

Zhou,Xiaofang, Zhou,Siwei, Li,Yuanmei, Qian,Zhiyong, Zeng,Chao, and Li,Yang

Subjects
Male, Angiotensin II, NF-kappa B, Endothelial Cells, NADPH Oxidases, Medicine (miscellaneous), Coronary Disease, General Medicine, Atherosclerosis, Mice, Oxidative Stress, Human Umbilical Vein Endothelial Cells, Animals, Humans, Surgery, Cardiology and Cardiovascular Medicine, Reactive Oxygen Species, Signal Transduction, Transcription Factors, Coronary Diseases
Abstract

Introduction: Coronary heart disease (CHD) is a dynamic process in which there are interactions between endothelial dysfunction, oxidative stress, and inflammatory responses. The aim of the present study was to investigate the function and mechanism of HSCARG in the treatment of CHD. Methods: Male apolipoprotein E/low-density lipoprotein receptor-deficient mice were given a high-fat diet with 21% fat and 0.15% cholesterol for the in vivo model. Human umbilical vein endothelial cells were incubated with angiotensin II for the in vitro model. HSCARG expression was inhibited in patients or mice with CHD. Results: HSCARG reduced oxidative stress in mice with CHD. HSCARG also reduced reactive oxygen species (ROS)-oxidative stress in the in vitro model. HSCARG induced p47phox expression in the in vitro model by NF-κB activity. The regulation of nuclear factor kappa B (NF-κB) activity or p47phox expression participates in the effects of HSCARG in CHD. Conclusion: Altogether, our data indicate that HSCARG reduced ROS-oxidative stress in in vivo and in vitro models of CHD via p47phox by NF-κB activity and may be a clinical target for CHD.

Published
2022

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