淋巴细胞中的瞬时受体电位通道

TRP channels in lymphocytes.

作者信息

Schwarz E C, Wolfs M J, Tonner S, Wenning A S, Quintana A, Griesemer D, Hoth M

机构信息

Institut für Physiologie, Universität des Saarlandes, Gebäude 58, 66421 Homburg/Saar, Germany.

出版信息

Handb Exp Pharmacol. 2007(179):445-56. doi: 10.1007/978-3-540-34891-7_26.

DOI:10.1007/978-3-540-34891-7_26

PMID:17217072

Abstract

TRP proteins form ion channels that are activated following receptor stimulation. Several members of the TRP family are likely to be expressed in lymphocytes. However, in many studies, messenger RNA (mRNA) but not protein expression was analyzed and cell lines but not primary human or murine lymphocytes were used. Among the expressed TRP mRNAs are TRPC1, TRPC3, TRPM2, TRPM4, TRPM7, TRPV1, and TRPV2. Regulation of Ca2+ entry is a key process for lymphocyte activation, and TRP channels may both increase Ca2+ influx (such as TRPC3) or decrease Ca2+ influx through membrane depolarization (such as TRPM4). In the future, linking endogenous Ca2+/cation channels in lymphocytes with TRP proteins should lead to a better molecular understanding of lymphocyte activation.

摘要

瞬时受体电位（TRP）蛋白形成在受体刺激后被激活的离子通道。TRP家族的几个成员可能在淋巴细胞中表达。然而，在许多研究中，仅分析了信使核糖核酸（mRNA）而非蛋白表达，并且使用的是细胞系而非原代人或小鼠淋巴细胞。在表达的TRP mRNA中，有TRPC1、TRPC3、TRPM2、TRPM4、TRPM7、TRPV1和TRPV2。钙离子（Ca2+）内流的调节是淋巴细胞激活的关键过程，TRP通道既可能增加Ca2+内流（如TRPC3），也可能通过膜去极化减少Ca2+内流（如TRPM4）。未来，将淋巴细胞中的内源性Ca2+/阳离子通道与TRP蛋白联系起来，应该能在分子层面更好地理解淋巴细胞激活。