Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2010 Jun 1;15(3):1023-39.
doi: 10.2741/3660.

TRPC channels in smooth muscle cells

Jose C Gonzalez-Cobos  1 , Mohamed Trebak
Affiliations
Review

TRPC channels in smooth muscle cells

Jose C Gonzalez-Cobos et al. Front Biosci (Landmark Ed). .

Abstract

Transient receptor potential canonical (TRPC) proteins constitute a family of seven (TRPC1-7) nonselective cation channels within the wider TRP superfamily. TRPC1, TRPC3, TRPC4, TRPC5 and TRPC6 channels are expressed in vascular smooth muscle cells from human vessels of all calibers and in smooth muscle from organs such as the uterus and the gastrointestinal tract. TRPC channels have recently emerged as important players in the control of smooth muscle function. This review will focus on the retrospective analysis of studies proposing contributions of TRPC channels to native calcium entry pathways in smooth muscle and to physiological and pathophysiological responses with emphasis on the vascular system.

PubMed Disclaimer

Figures

Figure 1
Figure 1. TRPC-mediated signaling in smooth muscle cells
The engagement of a vasoactive compound/growth factor receptor in vascular smooth muscle cells leads to the activation of phospholipase C (PLC) which catalyzes the breakdown of phosphatidylinositol 4,5-bisphosphate (PIP2) into two intracellular second messengers, the Inositol 1,4,5-trisphosphate (IP3) and Diacylglycerol (DAG). IP3-mediated Ca2+ store depletion activates store-operated Orai1 channels in a mechanism dependent on STIM1 aggregation and translocation into areas of close SR-PM contacts. The role of TRPC channels in mediating SOC channels remains to this day a highly contentious issue. All TRPC are activated by mechanisms downstream of PLC; TRPC3/6/7 have been shown to be activated by DAG in a PKC independent manner while TRPC1/4/5 exact mechanisms of activation via membrane receptors is still unclear and seems to involve PIP2 breakdown and Ca2+. Na+ entry through nonselective TRPC channels has been proposed to couple to activation of Ca2+ entry either through the Na+/Ca2+ exchanger (NCX) or via depolarization and subsequent activation of L-type Ca2+ channels. Increasing evidence supports a signaling paradigm in which Ca2+ signals mediated by specific TRPC isoforms are able to activate transcription factors in smooth muscle that act to increase the corresponding TRPC channel expression.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Barritt GJ. Receptor-activated Ca2+ inflow in animal cells: a variety of pathways tailored to meet different intracellular Ca2+ signalling requirements. Biochem J. 1999;337(Pt 2):153–69. - PMC - PubMed
    1. Berridge MJ. Smooth muscle cell calcium activation mechanisms. J Physiol. 2008;586:5047–61. - PMC - PubMed
    1. Berridge MJ, Lipp P, Bootman MD. The versatility and universality of calcium signalling. Nat Rev Mol Cell Biol. 2000;1:11–21. - PubMed
    1. Berridge MJ. Calcium microdomains: organization and function. Cell Calcium. 2006;40:405–12. - PubMed
    1. House SJ, Potier M, Bisaillon J, Singer HA, Trebak M. The non-excitable smooth muscle: calcium signaling and phenotypic switching during vascular disease. Pflugers Arch. 2008;456:769–85. - PMC - PubMed

Publication types

Substances

LinkOut - more resources