Regulatory effect of connexin 43 on basal Ca2+ signaling in rat ventricular myocytes.

PloS One
Chen LiDali Luo

Abstract

It has been found that gap junction-associated intracellular Ca(2+) [Ca(2+)](i) disturbance contributes to the arrhythmogenesis and hyperconstriction in diseased heart. However, whether functional gaps are also involved in the regulation of normal Ca(2+) signaling, in particular the basal [Ca(2+)](i) activities, is unclear. Global and local Ca(2+) signaling and gap permeability were monitored in cultured neonatal rat ventricular myocytes (NRVMs) and freshly isolated mouse ventricular myocytes by Fluo4/AM and Lucifer yellow (LY), respectively. The results showed that inhibition of gap communication by heptanol, Gap 27 and flufenamic acid or interference of connexin 43 (Cx43) with siRNA led to a significant suppression of LY uptake and, importantly, attenuations of global Ca(2+) transients and local Ca(2+) sparks in monolayer NRVMs and Ca(2+) sparks in adult ventricular myocytes. In contrast, overexpression of rat-Cx43 in NRVMs induced enhancements in the above measurements, and so did in HEK293 cells expressing rat Cx43. Additionally, membrane-permeable inositol 1,4,5-trisphosphate (IP(3) butyryloxymethyl ester) and phenylephrine, an agonist of adrenergic receptor, could relieve the inhibited Ca(2+) signal and LY uptake by gap u...Continue Reading

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Mar 20, 2014·Human Reproduction Update·Sofia MakievaJane E Norman
Apr 2, 2015·Journal of Molecular and Cellular Cardiology·Karin P HammerDonald M Bers
Jan 30, 2013·Pharmacology & Therapeutics·Romain GuinamardChristopher Del Negro
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Jul 9, 2017·The American Journal of Pathology·Lisa PrevedelEliseo A Eugenin

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Methods Mentioned

BETA
confocal microscopy
PCR
transfection
fluorescence recovery after bleaching

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