MiR-665 aggravates heart failure via suppressing CD34-mediated coronary microvessel angiogenesis.

ABSTRACT:

Background

Heart failure (HF) is a major public health problem worldwide. The development of HF was related to coronary microvessel dysfunction. Whether miRNAs participate in HF by regulating coronary microvessel function remain unclear.

Methods

The potential targets of miR-665 were predicted by rnahybrid software, then verified through anti-Ago2 co-immunoprecipitation, Western blotting and luciferase reporter assays. rAAV9 system was used to manipulate the expression of miR-665 in vivo.

Results

Significant increase of miR-665 was observed in endothelial cells of human heart with heart failure. In vitro over-expression of miR-665 in endothelial cells resulted in decreased proliferation but enhanced apoptosis. rAAV-mediated delivery of miR-665 reduced coronary microves

SUBMITTER: Fan J 

PROVIDER: S-EPMC6188485 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature