HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 292/1/C553    most recent 00096.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Morales, S. Articles by Pozo, M. J. Search for Related Content PubMed PubMed Citation Articles by Morales, S. Articles by Pozo, M. J.

RECEPTORS AND SIGNAL TRANSDUCTION

Calcium controls smooth muscle TRPC gene transcription via the CaMK/calcineurin-dependent pathways

¹Department of Physiology, University of Extremadura, Cáceres; ²Department of Biochemistry and Molecular Biology IV, University Complutense of Madrid, Madrid, Spain

Submitted 1 March 2006 ; accepted in final form 30 August 2006

Transient receptor potential protein family C (TRPC) has been proposed as a candidate for channels involved in capacitative Ca²⁺ entry (CCE) mechanisms, but the modulation of their gene expression remains unexplored. In this study we show that guinea pig gallbladder smooth muscle contains mRNA encoding TRPC1, TRPC2, TRPC3, and TRPC4 proteins whose abundance depends on cytosolic Ca²⁺ level ([Ca²⁺]_i). Thus lowering the levels of cellular calcium with the chelators EGTA and BAPTA AM results in a downregulation of TRPC1–TRPC4 gene and protein expression. In contrast, activation of Ca²⁺ influx through L-type Ca²⁺ channels and Ca²⁺ release from intracellular stores induced an increase in TRPC1–TRPC4 mRNA and protein abundance. Activation of Ca²⁺/calmodulin-dependent kinases (CaMK) and phosphorylation of cAMP-response element binding protein accounts for the increase in TRPC mRNA transcription in response to L-type channel-mediated Ca²⁺ influx . In addition to this mechanism, activation of TRPC gene expression by intracellular Ca²⁺ release also involves calcineurin pathway. According to the proposed role for these channels, activation of CCE induced an increase in TRPC1 and TRPC3 mRNA abundance, which depends on the integrity of the calcineurin and CaMK pathways. These findings show for the first time an essential autoregulatory role of Ca²⁺ in Ca²⁺ homeostasis at the level of TRPC gene and protein expression.

transient receptor protein family C channels; cytosolic calcium levels; gallbladder

This article has been cited by other articles:

				Y Shi, X Ding, Z-H He, K-C Zhou, Q Wang, and Y-Z Wang Critical role of TRPC6 channels in G2 phase transition and the development of human oesophageal cancer Gut, November 1, 2009; 58(11): 1443 - 1450. [Abstract] [Full Text] [PDF]

				M. Irnaten, R. C. Barry, B. Quill, A. F. Clark, B. J. P. Harvey, and C. J. O'Brien Activation of Stretch-Activated Channels and Maxi-K+ Channels by Membrane Stress of Human Lamina Cribrosa Cells Invest. Ophthalmol. Vis. Sci., January 1, 2009; 50(1): 194 - 202. [Abstract] [Full Text] [PDF]

				K. M. Lounsbury Preventing Stenosis by Local Inhibition of KCa3.1: A Finger on the Phenotypic Switch Arterioscler Thromb Vasc Biol, June 1, 2008; 28(6): 1036 - 1038. [Full Text] [PDF]

				J. R. Kovac, T. Chrones, and S. M. Sims Temporal and spatial dynamics underlying capacitative calcium entry in human colonic smooth muscle Am J Physiol Gastrointest Liver Physiol, January 1, 2008; 294(1): G88 - G98. [Abstract] [Full Text] [PDF]