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- 저자 : Qingqing Tan (검색결과 3 건)
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Wang Bo,Tan Yong,Zhang Yunkai,Zhang Sheng,Duan Xuewen,Jiang Yuyu,Li Tong,Zhou Qingqing,Liu Xingguang,Zhan Zhenzhen 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Excessive cardiac fibrosis is central to adverse cardiac remodeling and dysfunction leading to heart failure in many cardiac diseases. Histone methylation plays a crucial role in various pathophysiological events. However, the role of histone methylation modification enzymes in pathological cardiac fibrosis needs to be fully elucidated. Here, we identified lysine demethylase 5B (KDM5B), a histone H3K4me2/me3 demethylase, as a key epigenetic mediator of pathological cardiac fibrosis. KDM5B expression was upregulated in cardiac fibroblasts and myocardial tissues in response to pathological stress. KDM5B deficiency markedly ameliorated cardiac fibrosis, improved cardiac function, and prevented adverse cardiac remodeling following myocardial infarction (MI) or pressure overload. KDM5B knockout or inhibitor treatment constrained the transition of cardiac fibroblasts to profibrogenic myofibroblasts and suppressed fibrotic responses. KDM5B deficiency also facilitated the transformation of cardiac fibroblasts to endothelial-like cells and promoted angiogenesis in response to myocardial injury. Mechanistically, KDM5B bound to the promoter of activating transcription factor 3 (Atf3), an antifibrotic regulator of cardiac fibrosis, and inhibited ATF3 expression by demethylating the activated H3K4me2/3 modification, leading to the enhanced activation of TGF-β signaling and excessive expression of profibrotic genes. Our study indicates that KDM5B drives pathological cardiac fibrosis and represents a candidate target for intervention in cardiac dysfunction and heart failure.
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Qian Liu,Bishao Sun,Jiang Zhao,Qingqing Wang,Fan An,Xiaoyan Hu,Zhenxing Yang,Jie Xu,Mingjia Tan,Longkun Li 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
The Piezo1 channel is a mechanotransduction mediator, and Piezo1 abnormalities have been linked to several clinical disorders. However, the role of the Piezo1 channel in cystitis-associated bladder dysfunction has not been documented. The current study aimed to discover the functional role of this channel in regulating bladder activity during cyclophosphamide (CYP)-induced cystitis. One hundred four female rats were randomly assigned to the control, CYP-4h, CYP-48h and CYP-8d groups. CYP successfully induced acute or chronic cystitis in these rats. CYP treatment for 48h or 8d significantly increased Piezo1 channel expression in bladder interstitial Cajal-like cells (ICC-LCs), and the increase in CYP-8d rats was more prominent. In addition, 2.5 μM Grammostola spatulata mechanotoxin 4 (GsMTx4) significantly attenuated bladder hyperactivity in CYP-8d rats by inhibiting the Piezo1 channel in bladder ICCLCs. Furthermore, by using GsMTx4 and siRNA targeting the Piezo1 channel, we demonstrated that hypotonic stressinduced Piezo1 channel activation significantly triggered Ca2+ and Na+ influx into bladder ICC-LCs during CYPinduced chronic cystitis. In addition, the Piezo1 channel functionally interacted with the relatively activated reverse mode of Na+/Ca2+ exchanger 1 (NCX1) in bladder ICC-LCs from CYP-8d rats. In conclusion, we suggest that the functional role of the Piezo1 channel in CYP-induced chronic cystitis is based on its synergistic effects with NCX1, which can significantly enhance [Ca2+]i and result in Ca2+ overload in bladder ICC-LCs, indicating that the Piezo1 channel and NCX1 are potential novel therapeutic targets for chronic cystitis-associated bladder hyperactivity.
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Transcriptomic Features of Echinococcus granulosus Protoscolex during the Encystation Process
Junjie Fan,Hongye Wu,Kai Li,Xunuo Liu,Qingqing Tan,Wenqiao Cao,Bo Liang,Bin Ye 대한기생충학ㆍ열대의학회 2020 The Korean Journal of Parasitology Vol.58 No.3
Cystic echinococcosis (CE) is a zoonotic infection caused by Echinococcus granulosus larvae. It seriously af- fects the development of animal husbandry and endangers human health. Due to a poor understanding of the cystic fluid formation pathway, there is currently a lack of innovative methods for the prevention and treatment of CE. In this study, the protoscoleces (PSCs) in the encystation process were analyzed by high-throughput RNA sequencing. A total of 32,401 transcripts and 14,903 cDNAs revealed numbers of new genes and transcripts, stage-specific genes, and differ- ently expressed genes. Genes encoding proteins involved in signaling pathways, such as putative G-protein coupled re- ceptor, tyrosine kinases, and serine/threonine protein kinase, were predominantly up-regulated during the encystation process. Antioxidant enzymes included cytochrome c oxidase, thioredoxin glutathione, and glutathione peroxidase were a high expression level. Intriguingly, KEGG enrichment suggested that differentially up-regulated genes involved in the va- sopressin-regulated water reabsorption metabolic pathway may play important roles in the transport of proteins, carbo- hydrates, and other substances. These results provide valuable information on the mechanism of cystic fluid production during the encystation process, and provide a basis for further studies on the molecular mechanisms of growth and de- velopment of PSCs.
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