Loss of O‐GlcNAc transferase activity sensitizes cardiac myocytes to post‐hypoxic death

• DOI: 10.1096/fasebj.22.1_supplement.750.10
• Publication Date: 2021-06-21T23:30:39Z
• Authors: Gladys Afor Ngoh; Lewis J. Watson; Steven P. Jones
• Keywords: 0301 basic medicine; 03 medical and health sciences; 3. Good health

We recently reported that diabetic hearts have a paradoxical reduction in β‐ O ‐linked‐N‐acetylglucosamine ( ‐GlcNAc) signaling. Because enhancement of ‐GlcNAc signaling is cardioprotective, we hypothesized loss OGT activity sufficient to sensitize nondiabetic cardiac myocytes post‐hypoxic injury. Here, loxP‐ flanked neonatal mouse (n=3/group) were infected with an adenovirus carrying cre recombinase gene (AdCre, 72hours; 50 moi). Expression reduced expression (44+/−16%, p<0.05) and levels (28+/−5%, p< 0.05) according western blotting. Furthermore, such transcriptional silencing significantly (122+/−7%, exacerbated injury LDH release. To further confirm these findings, rat transfected 30nM siRNA, knockdown OGT. siRNA‐treatment (49+/−8%, (75+/−13%, compared control siRNA. Such decrement corresponded release (120+/−2%, p<0.05). conclude diminishes sensitizes lethal cell insights support the hypothesis defects are at least partially responsible for sensitivity myocardium ischemia‐reperfusion Moreover, basal elemental ability withstand hypoxic NIH (HL0833220), AHA (0535270N) (0715493B).