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Am J Physiol Lung Cell Mol Physiol (June 3, 2005). doi:10.1152/ajplung.00134.2005
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Submitted on March 23, 2005
Accepted on May 20, 2005

REGULATION OF Rho/ROCK SIGNALING IN AIRWAY SMOOTH MUSCLE BY MEMBRANE POTENTIAL AND [Ca2+]i

Caiqiong Liu1, Jianmin Zuo1, Evi Pertens1, Peter B. Helli1, and Luke J. Janssen1*

1 Medicine, McMaster University, Hamilton, ON, Canada

* To whom correspondence should be addressed. E-mail: janssenl{at}mcmaster.ca.

Recently, we have shown that Rho and Rho-kinase (ROCK) may become activated by high millimolar KCl, which had previously been widely assumed to act solely through opening of voltage-dependent Ca2+ channels. In this study, we explored in more detail the relationship between membrane depolarization, Ca2+currents and activation of Rho/ROCK in bovine tracheal smooth muscle. Ca2+ currents began to activate at membrane voltages more positive than -40 mV, and were maximally activated above 0 mV; at the same time, these underwent time- and voltage-dependent inactivation. Depolarizing intact tissues by KCl-challenge evoked contractions which were blocked equally, and in a non-additive fashion, by nifedipine or by the ROCK inhibitor Y27632. Other agents which elevate [Ca2+]i by pathways independent of G-protein coupled receptors (namely the SERCA-pump inhibitor cyclopiazonic acid and the Ca2+-ionophore A23187) evoked contractions that were also largely reduced by Y27632. KCl directly increased Rho- and ROCK-activities in a concentration-dependent fashion which paralleled closely the effect of KCl on tone and [Ca2+]i, as well as the voltage-dependent Ca2+-currents which were measured over the voltage ranges which are evoked by 0-120 mM KCl. Through the use of various pharmacological inhibitors, we ruled out roles for Ca2+/calmodulin-dependent Cam kinase II, protein kinase C and protein kinase A in mediating the KCl-stimulated changes in tone and Rho/ROCK activities. In conclusion, Rho is activated by elevation of [Ca2+]i (although the signal transduction pathway underlying this Ca2+-dependence is still unclear) and possibly also by membrane depolarization per se.




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