Cardiac Developmental Biology

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RhoA GTPase regulates L-type Ca²⁺ currents in cardiac myocytes

Atsuko Yatani; Keiichi Irie; Takayuki Otani; Maha Abdellatif; Lei Wei (Profiled Author: Lei Wei)

American Journal of Physiology - Heart and Circulatory Physiology. 2005;288(2 57-2):H650-H659.

Regulation of ionic channels plays a pivotal role in controlling cardiac function. Here we show that the Rho family of small G proteins regulates L-type Ca²⁺ currents in ventricular cardiomyocytes. Ventricular myocytes isolated from transgenic (TG) mice that overexpress the specific GDP dissociation inhibitor Rho GDI-α exhibited significantly decreased basal L-type Ca²⁺ current density (∼40%) compared with myocytes from nontransgenic (NTG) mice. The Ca²⁺ channel agonist BAY K 8644 and the β-adrenergic agonist isoproterenol increased Ca²⁺ currents in both NTG and TG myocytes to a similar maximal level, and no changes in mRNA or protein levels were observed in the Ca²⁺ channel α1- subunits. These results suggest that the channel activity but not the expression level was altered in TG myocytes. In addition, the densities of inward rectifier and transient outward K⁺ currents were unchanged in TG myocytes. The amplitudes and rates of basal twitches and Ca²⁺ transients were also similar between the two groups. When the protein was delivered directly into adult ventricular myocytes via TAT-mediated protein transduction, Rho GDI-α significantly decreased Ca²⁺ current density, which supports the idea that the defective Ca²⁺ channel activity in TG myocytes was a primary effect of the transgene. In addition, expression of a dominant-negative RhoA but not a dominant-negative Rac-1 or Cdc42 also significantly decreased Ca²⁺ current density, which indicates that inhibition of Ca²⁺ channel activity by overexpression of Rho GDI-α is mediated by inhibition of RhoA. This study points to the L-type Ca²⁺ channel activity as a novel downstream target of the RhoA signaling pathway.

PMID: 15471984    

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