Open AccessActivation of transient receptor potential vanilloid 3 channel ( TRPV 3) aggravated pathological cardiac hypertrophy via calcineurin/ NFAT c3 pathway in rats
Author(s) -
Zhang Qianhui,
Qi Hanping,
Cao Yonggang,
Shi Pilong,
Song Chao,
Ba Lina,
Chen Yunping,
Gao Jingquan,
Li Shuzhi,
Li Baiyan,
Sun Hongli
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13880
Subject(s) - trpv , nfat , transient receptor potential channel , endocrinology , calcineurin , medicine , chemistry , muscle hypertrophy , myocyte , microbiology and biotechnology , trpv1 , biology , receptor , transplantation
Cardiac hypertrophy is a compensatory response to mechanical stimuli and neurohormonal factors, ultimately progresses to heart failure. The proteins of some transient receptor potential ( TRP ) channels, Ca 2+ ‐permeable nonselective cation channel, are highly expressed in cardiomyocytes, and associated with the occurrence of cardiac hypertrophy. Transient receptor potential vanilloid 3 ( TRPV 3) is a member of TRP , however, the functional role of TRPV 3 in cardiac hypertrophy remains unclear. TRPV 3 was elevated in pathological cardiac hypertrophy, but not in swimming exercise‐induced physiological cardiac hypertrophy in rats. TRPV 3 expression was also increased in Ang II –induced cardiomyocyte hypertrophy in vitro, which was remarkably increased by carvacrol (a nonselective TRPV channel agonist), and reduced by ruthenium red (a nonselective TRPV channel antagonist). Interestingly, we found that activated TRPV 3 in Ang II –induced cardiomyocyte hypertrophy was accompanied with increasing intracellular calcium concentration, promoting calcineurin, and phosphorylated Ca MKII protein expression, and enhancing NFAT c3 nuclear translocation. However, blocking or knockdown of TRPV 3 could inhibit the expressions of calcineurin, phosphorylated Ca MKII and NFAT c3 protein by Western blot. In conclusion, the activation of TRPV 3 aggravated pathological cardiac hypertrophy through calcineurin/ NFAT c3 signalling pathway and correlated with the protein expression levels of calcineurin, phosphorylated Ca MKII and NFAT c3, revealing that TRPV 3 might be a potential therapeutic target for cardiac hypertrophy.