MicroRNA-126 regulates endothelial expression of vascular cell adhesion molecule 1

MicroRNA-126 regulates endothelial expression of vascular cell adhesion molecule 1

February 5, 2008 | Tamia A. Harris*, Munekazu Yamakuchi†, Marcella Ferlito†, Joshua T. Mendell†§∥, and Charles J. Lowenstein*†∥**
The study investigates the role of microRNA-126 (miR-126) in regulating vascular cell adhesion molecule 1 (VCAM-1) expression in endothelial cells. VCAM-1 is an important adhesion molecule that mediates leukocyte adherence to endothelial cells, which is crucial for leukocyte trafficking to sites of inflammation. The authors found that miR-126 is selectively expressed in endothelial cells and inhibits VCAM-1 expression. They demonstrated that decreasing miR-126 levels in endothelial cells increases VCAM-1 expression and leukocyte adherence, while overexpressing miR-126 decreases VCAM-1 expression. In vitro experiments using reporter vectors and immunoblotting confirmed that miR-126 targets a specific region in the 3′-UTR of the VCAM-1 transcript, leading to its suppression. These findings suggest that miR-126 plays a key role in regulating vascular inflammation by controlling VCAM-1 expression.The study investigates the role of microRNA-126 (miR-126) in regulating vascular cell adhesion molecule 1 (VCAM-1) expression in endothelial cells. VCAM-1 is an important adhesion molecule that mediates leukocyte adherence to endothelial cells, which is crucial for leukocyte trafficking to sites of inflammation. The authors found that miR-126 is selectively expressed in endothelial cells and inhibits VCAM-1 expression. They demonstrated that decreasing miR-126 levels in endothelial cells increases VCAM-1 expression and leukocyte adherence, while overexpressing miR-126 decreases VCAM-1 expression. In vitro experiments using reporter vectors and immunoblotting confirmed that miR-126 targets a specific region in the 3′-UTR of the VCAM-1 transcript, leading to its suppression. These findings suggest that miR-126 plays a key role in regulating vascular inflammation by controlling VCAM-1 expression.
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