Transient receptor potential channels contribute to pathological structural and functional remodeling after myocardial infarction.

ABSTRACT:

Rationale

The cellular and molecular basis for post-myocardial infarction (MI) structural and functional remodeling is not well understood.

Objective

Our aim was to determine if Ca2+ influx through transient receptor potential canonical (TRPC) channels contributes to post-MI structural and functional remodeling.

Methods and results

TRPC1/3/4/6 channel mRNA increased after MI in mice and was associated with TRPC-mediated Ca2+ entry. Cardiac myocyte-specific expression of a dominant-negative (loss-of-function) TRPC4 channel increased basal myocyte contractility and reduced hypertrophy and cardiac structural and functional remodeling after MI while increasing survival in mice. We used adenovirus-mediated expression of TRPC3/4/6 channels in cultured adult feline myocytes

SUBMITTER: Makarewich CA 

PROVIDER: S-EPMC4149870 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature