Forced expression of miR-143 and -145 in cardiomyocytes induces cardiomyopathy with a reductive redox shift.

ABSTRACT:

Background

Animal model studies show that reductive stress is involved in cardiomyopathy and myopathy, but the exact physiological relevance remains unknown. In addition, the microRNAs miR-143 and miR-145 have been shown to be upregulated in cardiac diseases, but the underlying mechanisms associated with these regulators have yet to be explored.

Methods

We developed transgenic mouse lines expressing exogenous miR-143 and miR-145 under the control of the alpha-myosin heavy chain (αMHC) promoter/enhancer.

Results

The two transgenic lines showed dilated cardiomyopathy-like characteristics and early lethality with markedly increased expression of miR-143. The expression of hexokinase 2 (HK2), a cardioprotective gene that is a target of miR-143, was strongly suppressed in

SUBMITTER: Ogawa K 

PROVIDER: S-EPMC7444248 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature