Abstract
Transient receptor potential vanilloid family type 2 channels (TRPV2) is stretch-activated Ca2+ channels and localized to intercalated discs which are mechanical connections between two adjacent cardiomyocytes. However, the physiological roles of TRPV2 in cardiomyocytes remain unclear. Here, we generated cardiac-specific and temporally-controlled TRPV2 knock out (KO) mice using Cre-loxP system. Although cardiac pump function significantly dropped within 4 days of eliminating TRPV2 from adult hearts, morphological changes and intramuscular fibrosis of the hearts were not observed. Single cardiomyocytes isolated from the hearts showed no abnormalities in intracellular Ca2+ transients and contractilities evoked by electrical stimulations. However, the structure of intercalated discs was disrupted in TRPV2 KO mice, suggesting that the functional integration neighboring cardiomyocytes declined severely. These results suggest that TRPV2 is pivotal for the maintenance of intercalated discs and cardiac function in adult mice.
