MiR-320a mediates doxorubicin-induced cardiotoxicity by targeting VEGF signal pathway.

ABSTRACT:

Background

Vascular homeostasis abnormalities may involve in doxorubicin induced cardiotoxicity.

Methods

Enhanced cardiac miR-320a expression, reduced cardiac microvessel density and impaired cardiac function were observed in mice treated by anthracycline doxorubicin. To further explore the role of miR-320a in doxorubicin induced cardiotoxicity, microRNA mimics/inhibitor in vitro and rAAV administration in vivo were employed in mice.

Results

Knockdown of miR-320a not only resulted in enhanced proliferation and inhibited apoptosis in cultured endothelial cells, but also attenuated cardiac abnormalities induced by doxorubicin. On the contrary, overexpression of miR-320a enhanced apoptosis in vitro, and aggravated vessel abnormalities in heart and subsequent cardiac dysf

SUBMITTER: Yin Z 

PROVIDER: S-EPMC4761722 | biostudies-literature | 2016 Jan

REPOSITORIES: biostudies-literature