Endocardial TRPC-6 Act as Atrial Mechanosensors and Load-Dependent Modulators of Endocardial/Myocardial Cross-Talk

Mechanoelectrical feedback may increase arrhythmia susceptibility, but the molecular mechanisms are incompletely understood. This study showed that mechanical stretch altered the localization, protein levels, and function of the cation-selective transient receptor potential channel (TRPC)-6 in atria...

Full description

Saved in:
Bibliographic Details
Published in:JACC. Basic to translational science 2017-10, Vol.2 (5), p.575-590
Main Authors: Vesna Nikolova-Krstevski, PhD, Soeren Wagner, MD, Ze Yan Yu, MD, Charles D. Cox, PhD, Jasmina Cvetkovska, BSc, Adam P. Hill, PhD, Inken G. Huttner, MD, Victoria Benson, PhD, Andreas A. Werdich, PhD, Calum MacRae, MD, PhD, Michael P. Feneley, MD, PhD, Oliver Friedrich, PhD, Boris Martinac, PhD, Diane Fatkin, MD
Format: Article
Language:English
Subjects:
atrial endocardium
endothelium
mechanical stretch
transient receptor potential channels
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Mechanoelectrical feedback may increase arrhythmia susceptibility, but the molecular mechanisms are incompletely understood. This study showed that mechanical stretch altered the localization, protein levels, and function of the cation-selective transient receptor potential channel (TRPC)-6 in atrial endocardial cells in humans, pigs, and mice. In endocardial/myocardial cross-talk studies, addition of media from porcine atrial endocardium (AE) cells altered the calcium (Ca2+) transient characteristics of human-induced pluripotent stem cell-derived cardiomyocytes. These changes did not occur with media from stretched AE cells. Our data suggested that endocardial TRPC-6-dependent paracrine signaling may modulate myocardial Ca2+ homeostasis under basal conditions and protect against stretch-induced atrial arrhythmias.
ISSN:2452-302X
2452-302X
DOI:10.1016/j.jacbts.2017.05.006