Deficiency of 1 integrins results in increased myocardial dysfunction after myocardial infarction

Prasanna Krishnamurthy ¹, Venkateswaran Subramanian ¹, Mahipal Singh ¹ and Krishna Singh ^1*

¹ East Tennessee State University, United States

^* To whom correspondence should be addressed. E-mail: singhk{at}etsu.edu.

Accepted 24 February 2006

Abstract

Objective: To study the role of 1 integrins in left ventricular (LV) remodeling after myocardial infarction (MI).

Methods and Results: LV structural and functional alterations were determined in wild-type (WT) and 1 integrin heterozygous knockout (hKO) mice 1 month post MI. MI increased 1 integrin expression in both groups, however, the increase was lower in hKO. Infarct size was similar in WT and hKO mice, whereas lung wet weight/dry weight ratio was increased in the hKO-MI mice (P<0.05 vs WT-MI). LV end-systolic and end- diastolic diameters were significantly higher, whereas percent fractional shortening was significantly lower in hKO-MI. The ratio of peak velocity of early LV filling (E wave) to that of the late LV filling (A wave) and the isovolumic relaxation time (IVRT) were increased in both MI groups. However, the increase in IVRT was significantly higher in the hKO-MI group versus WT-MI. Langendorff-perfusion analysis indicated reduced peak LV developed pressure (LVDP) and increased LV end diastolic pressure (LVEDP) in both MI groups. The reduction in peak LVDP and increase in LVEDP was higher in hKO-MI (P<0.05 vs WT-MI). Increase in fibrosis was not different between the two MI groups. The increase in myocyte circumference was higher in hKO-MI group (P<0.001 vs WT-MI). The number of apoptotic myocytes was significantly higher in hKO-MI group versus WT-MI 3 days post MI. The number of necrotic myocytes was not different between the two MI groups.

Conclusion: 1 integrins play a crucial role in post-MI remodeling with effects on left ventricular function, hypertrophy and apoptosis.

Keywords: Apoptosis, Heart failure, Integrin, Myocardium

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