Hypoxic induction of T-type Ca(2+) channels in rat cardiac myocytes: role of HIF-1α and RhoA/ROCK signalling

The Journal of Physiology
P González-RodríguezA Castellano

Abstract

T-type Ca(2+) channels are expressed in the ventricular myocytes of the fetal and perinatal heart, but are normally downregulated as development progresses. Interestingly, however, these channels are re-expressed in adult cardiomyocytes under pathological conditions. We investigated low voltage-activated T-type Ca(2+) channel regulation in hypoxia in rat cardiomyocytes. Molecular studies revealed that hypoxia induces the upregulation of Cav 3.2 mRNA, whereas Cav 3.1 mRNA is not significantly altered. The effect of hypoxia on Cav 3.2 mRNA was time- and dose-dependent, and required hypoxia inducible factor-1α (HIF-1α) stabilization. Patch-clamp recordings confirmed that T-type Ca(2+) channel currents were upregulated in hypoxic conditions, and the addition of 50 μm NiCl2 (a T-type channel blocker) demonstrated that the Cav 3.2 channel is responsible for this upregulation. This increase in current density was not accompanied by significant changes in the Cav 3.2 channel electrophysiological properties. The small monomeric G-protein RhoA and its effector Rho-associated kinase I (ROCKI), which are known to play important roles in cardiovascular physiology, were also upregulated in neonatal rat ventricular myocytes subjected to hypox...Continue Reading

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Citations

Jan 20, 2019·Journal of Cell Science·Lisa LeinhosAnke Zieseniss
Nov 28, 2018·Pediatric Cardiology·Shi-Min Yuan
Oct 27, 2017·PloS One·Chaymae El AlaouiPhilippe Lory
Jan 19, 2018·Cancer Research·Marta C SallánCarles Cantí
Apr 11, 2020·Biochimica Et Biophysica Acta. Reviews on Cancer·Lía AlzaCarles Cantí
Aug 3, 2021·Frontiers in Cardiovascular Medicine·Natalie N Khalil, Megan L McCain

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