TRP channels in uterine pathophysiology- A short review

J. R. Dash
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Abstract

Calcium ions are major upstream signalling molecules to initiate myogenic contraction. TRP (Transient receptor potential) proteins belong to cation channel protein family and are localized in the cell membrane. The most perform of TRPC is to control the inflow of Ca / Na batting on PKC pathway activation evoked by G-protein-coupled receptors (GPCR). TRPV6, is mostly expressed in pregnant uterus in human, mouse, rat and pig. TRPV6 and TRPC1 are related to embryo implantation. Upregulated TRPC3 urged to play an important role in LPS-induced preterm labor. TRPC1 and TRPM7 are rumoured to related to abnormal uterine fibroid contraction. TRPV4 channels are present within the pregnant and nonpregnant mouse uteri, and their activation by prostaglandin increases myometrial contractility. TRPA1 over activity could also be related to pre-eclampsia and connected cardiovascular diseases. So with growing evidences of upregulation of varied TRP proteins in several pathological conditions of the uterus in human and experimental animals signifies TRP proteins rising as a new therapeutic target in uterine pathophysiology.
子宫病理生理中TRP通道的研究综述
钙离子是引发肌原性收缩的主要上游信号分子。瞬时受体电位(TRP)蛋白属于阳离子通道蛋白家族,定位于细胞膜。TRPC最主要的作用是控制Ca / Na流入对g蛋白偶联受体(GPCR)激活PKC通路的影响。TRPV6,主要在人、小鼠、大鼠和猪的妊娠子宫中表达。TRPV6和TRPC1与胚胎着床有关。上调的TRPC3在lps诱导的早产中发挥重要作用。传言TRPC1和TRPM7与子宫肌瘤异常收缩有关。TRPV4通道存在于怀孕和未怀孕的小鼠子宫内,前列腺素激活它们可增加子宫肌收缩力。TRPA1过度活动也可能与先兆子痫和相关心血管疾病有关。因此,随着越来越多的证据表明,各种TRP蛋白在人和实验动物的子宫病理状态中上调,TRP蛋白在子宫病理生理中成为新的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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