Abstract
Nuclear transcription factor (NF)-κB regulates inflammatory and immune responses by increasing the expression of specific inflammatory genes in various tissues. Whether the infarcted heart includes the activation of NF-κB and a proinflammatory mediator cascade that it regulates has not been fully explored. Herein, we monitored the temporal and spatial activation of NF-κB, together with expression of tumor necrosis factor (TNF)-α, vascular cell adhesion molecule-1 (VCAM-1), and transforming growth factor (TGF)-β 1, in the infarcted rat heart at and remote to MI from day 3 to day 28 following left coronary artery ligation. Compared to the normal heart, we observed NF-κB activation, together with the elevated expression of VCAM-1 in endothelial cells, TNF-α and TGF-β 1 in inflammatory cells at sites of repair in the infarcted heart, which started on day 3, peaked on day 7, and gradually declined thereafter. Our findings suggest NF-κB activation and its proinflammatory mediator cascade are contributory to the inflammatory response and remodeling that appear at various sites of repair in the infarcted rat heart.
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