TY - JOUR
T1 - TRPC3 participates in angiotensin II type 1 receptor-dependent stress-induced slow increase in intracellular Ca2+ concentration in mouse cardiomyocytes
AU - Yamaguchi, Yohei
AU - Iribe, Gentaro
AU - Kaneko, Toshiyuki
AU - Takahashi, Ken
AU - Numaga-Tomita, Takuro
AU - Nishida, Motohiro
AU - Birnbaumer, Lutz
AU - Naruse, Keiji
N1 - Funding Information:
(JSPS KAKENHI 23300167, 26282121 and 16K12878 to G.I.), by the Intramural Research Program of the NIH (Project Z01-ES-101864 to L.B.) and by the Life Science Foundation of Japan (as a travel grant to Y.Y.).
Funding Information:
The authors would like to thank Ms. Keiko Kaihara (Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Japan) for her skilled technical support, and Dr. Anastasia Khokhlova (Ural Federal University, Institute of Immunology and Physiology, Russia) for her support in improving the method of myocyte isolation. The authors also thank Ms. Yumiko Morishita (Central Research Laboratory, Okayama University Medical School, Japan) for technical assistance with the histological preparations. This study was funded by the Japan Society for the Promotion of Science (JSPS KAKENHI 23300167, 26282121?and?16K12878 to G.I.), by the Intramural Research Program of the NIH (Project Z01-ES-101864 to L.B.) and by the Life Science Foundation of Japan (as a travel grant to Y.Y.).
Publisher Copyright:
© 2017, The Physiological Society of Japan and Springer Japan.
PY - 2018/3/1
Y1 - 2018/3/1
N2 - When a cardiac muscle is held in a stretched position, its [Ca2+] transient increases slowly over several minutes in a process known as stress-induced slow increase in intracellular Ca2+ concentration ([Ca2+]i) (SSC). Transient receptor potential canonical (TRPC) 3 forms a non-selective cation channel regulated by the angiotensin II type 1 receptor (AT1R). In this study, we investigated the role of TRPC3 in the SSC. Isolated mouse ventricular myocytes were electrically stimulated and subjected to sustained stretch. An AT1R blocker, a phospholipase C inhibitor, and a TRPC3 inhibitor suppressed the SSC. These inhibitors also abolished the observed SSC-like slow increase in [Ca2+]i induced by angiotensin II, instead of stretch. Furthermore, the SSC was not observed in TRPC3 knockout mice. Simulation and immunohistochemical studies suggest that sarcolemmal TRPC3 is responsible for the SSC. These results indicate that sarcolemmal TRPC3, regulated by AT1R, causes the SSC.
AB - When a cardiac muscle is held in a stretched position, its [Ca2+] transient increases slowly over several minutes in a process known as stress-induced slow increase in intracellular Ca2+ concentration ([Ca2+]i) (SSC). Transient receptor potential canonical (TRPC) 3 forms a non-selective cation channel regulated by the angiotensin II type 1 receptor (AT1R). In this study, we investigated the role of TRPC3 in the SSC. Isolated mouse ventricular myocytes were electrically stimulated and subjected to sustained stretch. An AT1R blocker, a phospholipase C inhibitor, and a TRPC3 inhibitor suppressed the SSC. These inhibitors also abolished the observed SSC-like slow increase in [Ca2+]i induced by angiotensin II, instead of stretch. Furthermore, the SSC was not observed in TRPC3 knockout mice. Simulation and immunohistochemical studies suggest that sarcolemmal TRPC3 is responsible for the SSC. These results indicate that sarcolemmal TRPC3, regulated by AT1R, causes the SSC.
KW - Angiotensin II type 1 receptor
KW - Ca handling
KW - Cardiomyocyte
KW - Mathematical model
KW - Stretch
KW - Transient receptor potential canonical 3
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U2 - 10.1007/s12576-016-0519-3
DO - 10.1007/s12576-016-0519-3
M3 - Article
C2 - 28105583
AN - SCOPUS:85009833951
SN - 1880-6546
VL - 68
SP - 153
EP - 164
JO - Journal of Physiological Sciences
JF - Journal of Physiological Sciences
IS - 2
ER -