Document Type

Article

Publication Date

Summer 6-24-2022

Abstract

Diabetes mellitus type 2 (DMT2) is a prevalent disease that affects many people throughout the world leading to issues such as diabetic cardiomyopathy. O-GlcNAcylation dysregulation, caused by increased levels of serum glucose, contributes to the pathophysiology of decreased cardiac function. O-GlcNAcylation modulates cardiac contraction by reacting with either serine or threonine residues. Our goal was to demonstrate the success of infection of adeno-associated virus 9 (AAV9) carrying the gene of alpha-cardiac actin (ACTC) mutated at Thr326. Here we show the expression of the mutant ACTC T326D in H9C2 cardiomyoblasts and HEK293T cell lines. Expression in H9C2 cells was significantly increased compared to WT and control. In addition, expression in HEK293T cells was significantly increased compared to the control. These results are promising in that the ACTC gene carried in AAV9 can be transduced into cells in diabetic mouse model to prevent O-GlcNAcylation and improve cardiac contractility.

Academic Level

medical student

Mentor/PI Department

Molecular Science

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