TRPV2 is critical for the maintenance of cardiac structure and function in mice

Yuki Katanosaka (), Keiichiro Iwasaki, Yoshihiro Ujihara, Satomi Takatsu, Koki Nishitsuji, Motoi Kanagawa, Atsushi Sudo, Tatsushi Toda, Kimiaki Katanosaka, Satoshi Mohri and Keiji Naruse
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Yuki Katanosaka: Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Keiichiro Iwasaki: Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Yoshihiro Ujihara: Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Satomi Takatsu: Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Koki Nishitsuji: Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Motoi Kanagawa: Kobe University Graduate School of Medicine
Atsushi Sudo: Kobe University Graduate School of Medicine
Tatsushi Toda: Kobe University Graduate School of Medicine
Kimiaki Katanosaka: Research Institute of Environmental Medicine, Nagoya University
Satoshi Mohri: Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Keiji Naruse: Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

Nature Communications, 2014, vol. 5, issue 1, 1-14

Abstract: Abstract The heart has a dynamic compensatory mechanism for haemodynamic stress. However, the molecular details of how mechanical forces are transduced in the heart are unclear. Here we show that the transient receptor potential, vanilloid family type 2 (TRPV2) cation channel is critical for the maintenance of cardiac structure and function. Within 4 days of eliminating TRPV2 from hearts of the adult mice, cardiac function declines severely, with disorganization of the intercalated discs that support mechanical coupling with neighbouring myocytes and myocardial conduction defects. After 9 days, cell shortening and Ca2+ handling by single myocytes are impaired in TRPV2-deficient hearts. TRPV2-deficient neonatal cardiomyocytes form no intercalated discs and show no extracellular Ca2+-dependent intracellular Ca2+ increase and insulin-like growth factor (IGF-1) secretion in response to stretch stimulation. We further demonstrate that IGF-1 receptor/PI3K/Akt pathway signalling is significantly downregulated in TRPV2-deficient hearts, and that IGF-1 administration partially prevents chamber dilation and impairment in cardiac pump function in these hearts. Our results improve our understanding of the molecular processes underlying the maintenance of cardiac structure and function.

Date: 2014
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DOI: 10.1038/ncomms4932

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