TRPV4 is not the molecular sensor for bacterial lipopolysaccharides-induced calcium signaling
文献类型：期刊论文
| 作者 | Wang, Yuhui2; Hao, Yanping3,4; Jin, Jinhua2; Yi, Zhihua6; Liu, Yifei3; Zhou, Huan3,4; Zhao, Guodun3,7; Wen, Lu; Dong, Huiqing3,7; Zhang, Yun3,7 |
| 刊名 | CELLULAR IMMUNOLOGY
 |
| 出版日期 | 2023 |
| 卷号 | 383页码:8 |
| ISSN号 | 0008-8749 |
| 关键词 | TRPV4 LPS Calcium influx Whole cell current Pain Inflammation |
| DOI | 10.1016/j.cellimm.2022.104651 |
| 通讯作者 | Wang, Ting(wangting@simm.ac.cn) ; Feng, Jing(fengjing@simm.ac.cn) |
| 英文摘要 | Lipopolysaccharides (LPS) is one of the most potent pathogen-associated signals for the immune system of vertebrates. In addition to the canonical pathway of LPS detection mediated by toll-like receptor 4 (TLR4) signaling pathway, TRP channel-mediated pathways endow sensory neurons and epithelial cells with the ability to detect and react to bacterial endotoxins. Previous work revealed that LPS triggers TRPV4-dependent calcium influx in urothelial cells (UCs) and mouse tracheobronchial epithelial cells (mTEC). In marked contrast, here we show that most subtypes of LPS could not directly activate TRPV4 channel. Although LPS from Salmonella enterica serotype Minnesota evoked a [Ca2+]i response in freshly isolated human bronchial epithelial cells (ECs), freshly isolated mouse ear skin single-cell suspensions, or HEK293T cells transiently transfected with mTRPV4, this activation occurred in a TRPV4-independent manner. Additionally, LPS from either E. coli strains or Salmonella enterica serotype Minnesota did not evoke significant difference in inflammation and pain hyperalgesia between wild type and TRPV4 deficient mice. In summary, our results demonstrate that in vitro and in vivo effects induced by LPS are independent of TRPV4, thus providing a clarity to the questioned role of LPS in TRPV4 activation. |
| WOS关键词 | ACTIVATION ; LPS ; INNATE |
| 资助项目 | National Natural Science Foundation of China[82171214] ; Lingang Laboratory[LG-QS-202203-07] |
| WOS研究方向 | Cell Biology ; Immunology |
| 语种 | 英语 |
| 出版者 | ACADEMIC PRESS INC ELSEVIER SCIENCE |
| WOS记录号 | WOS:000994306800001 |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/306581]  |
| 专题 | 中国科学院上海药物研究所 |
| 通讯作者 | Wang, Ting; Feng, Jing |
| 作者单位 | 1.Henan Univ, Sch Pharm, Kaifeng, Peoples R China 2.Chinese Acad Med Sci & Peking Union Med Coll, Dept Anesthesiol, Plast Surg Hosp, Beijing, Peoples R China 3.Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai, Peoples R China 4.Univ Chinese Acad Sci, Beijing, Peoples R China 5.Chinese Acad Sci, Shanghai Inst Mat Med, Ctr Neurol & Psychiat Res & Drug Discovery, 555 Zuchongzhi Rd, Shanghai 201203, Peoples R China 6.Nanchang Univ, Sch Nursing, Med Coll, Nanchang, Peoples R China 7.Nanjing Univ Chinese Med, Sch Chinese Mat Med, Nanjing, Peoples R China 8.Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Dept Plast & Reconstruct Surg, Div Reconstruct Microsurg,Sch Med China, Shanghai, Peoples R China |
| 推荐引用方式 GB/T 7714 | Wang, Yuhui,Hao, Yanping,Jin, Jinhua,et al. TRPV4 is not the molecular sensor for bacterial lipopolysaccharides-induced calcium signaling[J]. CELLULAR IMMUNOLOGY,2023,383:8. |
| APA | Wang, Yuhui.,Hao, Yanping.,Jin, Jinhua.,Yi, Zhihua.,Liu, Yifei.,...&Feng, Jing.(2023).TRPV4 is not the molecular sensor for bacterial lipopolysaccharides-induced calcium signaling.CELLULAR IMMUNOLOGY,383,8. |
| MLA | Wang, Yuhui,et al."TRPV4 is not the molecular sensor for bacterial lipopolysaccharides-induced calcium signaling".CELLULAR IMMUNOLOGY 383(2023):8. |
入库方式： OAI收割
来源：上海药物研究所
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