EphA2-receptor deficiency exacerbates myocardial infarction and reduces survival in hyperglycemic mice

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)

Anita Coburn (Creator)

Augustin DuSablon (Creator)

Susan Kent (Creator)

Jitka Virag (Creator)

Institution

East Carolina University (ECU )

Web Site: http://www.ecu.edu/lib/

Abstract: Background We have previously shown that EphrinA1/EphA expression profile changes in response to myocardial infarction (MI), exogenous EphrinA1-Fc administration following MI positively influences wound healing, and that deletion of the EphA2 Receptor (EphA2-R) exacerbates injury and remodeling. To determine whether or not ephrinA1-Fc would be of therapeutic value in the hyperglycemic infarcted heart, it is critical to evaluate how ephrinA1/EphA signaling changes in the hyperglycemic myocardium in response to MI. Methods Streptozotocin (STZ)-induced hyperglycemia in wild type (WT) and EphA2-receptor mutant (EphA2-R-M) mice was initiated by an intraperitoneal injection of STZ (150 mg/kg) 10 days before surgery. MI was induced by permanent ligation of the left anterior descending coronary artery and analyses were performed at 4 days post-MI. ANOVAs with Student-Newman Keuls multiple comparison post-hoc analysis illustrated which groups were significantly different, with significance of at least p?

Additional Information

Publication

Other

Cardiovascular Diabetology; 13: p. 1-16

Language: English

Date: 2014

Keywords

Diabetes, EphrinA1/EphA, Hyperglycemia, Ischemia, Myocardial infarction

Email this document to