Background— Integrins are involved in structural remodeling and tissue repair. This study aimed to elucidate the role of the β-integrins in cardiac remodeling after myocardial infarction (MI).

Methods and Results— The MI model was created by ligation of the left anterior descending coronary artery in rats. We detected cardiac integrins β1 and β3 gene expression (quantitative in situ hybridization) and protein production (Western blot and immunohistochemistry) and potential regulation by tumor necrosis factor (TNF) using neonatal ventricular myocytes and TNF^−/− knockout mice. Integrins β1 and β3 gene expression and protein production were low in sham-operated hearts. After MI, the β1 and β3 mRNA and proteins were significantly increased at the site of MI at day 3, reached a peak at day 7, and gradually declined thereafter. Integrin β1A localized primarily in fibroblasts and inflammatory cells, β1D localized in myocytes, and integrin β3 was associated primarily with endothelial and smooth muscle cells in peri-infarct vessels. In cultured myocytes, there was isoform transition from the adult β1D to the fetal β1A on exposure to TNF-α. This was confirmed in vivo in the peri-infarct myocytes, but the transition was voided in TNF^−/−-knockout mice.

Conclusions— Integrins β1 and β3 are significantly activated in the infarcted myocardium. Integrin β1 is active particularly at sites of inflammation and fibrosis, whereas integrin β3 localizes to vessels in the peri-infarct zone in a temporally coordinated manner. Integrin β1D to β1A isoform transition in myocytes is regulated by TNF-α.