Abstract
Small GTPase RhoA is critically involved in myocardial injury, repair, and fibrosis. However, the role of RhoA signaling in regulating of macrophage is poorly understand. In this study, we investigated the role of RhoA in macrophage in modulating cardiac function after myocardial infarction and dissected the mechanisms mediating RhoA dependent modulation of macrophage function. RhoA deletion in myeloid cells worsen the cardiac function and lead an increase in post-infarction scar and cardiac fibrosis. RhoA deletion in myeloid cells decreased CCR2 + infiltration in heart, however, increase the circulation of Ly6c hi monocytes in blood expression. RhoA deletion macrophage produce more pro-inflammatory cytokines IL-1β and IL-12b compared to control mice. Mechanistically, CCR2/RhoA axis is critical for CCl2 induced monocytes infiltration. We demonstrated RhoA critically regulates function of infarct macrophage by mediating CCL2 inducing macrophage infiltration and by contributing to proinflammatory transition.
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