DOI

https://doi.org/10.25772/25NX-YS97

Defense Date

2016

Document Type

Thesis

Degree Name

Master of Science

Department

Physiology and Biophysics

First Advisor

Edward Lesnefsky

Second Advisor

Robert Diegelmann

Third Advisor

Roland Pittman

Abstract

Type 2 diabetes mellitus is a growing problem across the world and has significant pathological changes associated with it, including diabetic cardiomyopathy, wherein cardiac function is reduced. MicroRNA-21 has been shown to play a role in both the heart and diabetes so it was thought that knocking out miR-21 could have a protective effect on oxidative phosphorylation function in diabetic mice. Subsarcolemmal and interfibrillar mitochondria were isolated from adult male WT, miR-21 KO, db/db, and double knockout mice (db/db and miR-21 KO cross) and evaluated for function. Knocking out miR-21 in diabetic mice showed a restorative effect in Complex I and Complex II function even though it increased ROS production in Complex I and did not show a significant change in MPTP opening. Knocking out miR-21 could potentially restore oxidative phosphorylation function in diabetic patients but at the expense of producing more ROS.

Rights

© The Author

Is Part Of

VCU University Archives

Is Part Of

VCU Theses and Dissertations

Date of Submission

5-10-2016

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