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

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EphA2-receptor deficiency exacerbates myocardial infarction and reduces survival in hyperglycemic micehttp://hdl.handle.net/10342/5799The described resource references, cites, or otherwise points to the related resource.