| dc.description.abstract | Fibrotic disorders, including atherosclerosis, are known to concur with endothelial-to-mesenchymal transition (EndMT) induced by cues from the tissue microenvironment such as transforming growth factor β (TGF-β). Nck, a family of adaptor proteins linking tyrosine phosphorylation with cytoskeletal remodeling, is involved in cardiovascular morphogenesis. Although EndMT underlies cardiovascular development, a potential role for Nck in TGF-β-induced EndMT is yet to be determined. To address this gap in the knowledge, naïve human umbilical vein endothelial cells (HUVEC) or HUVEC with short interference RNA (siRNA)-mediated silencing of Nck were left untreated or treated with TGF-β2 for 48 hours. Expression levels of Nck, endothelial and mesenchymal cell markers were determined by western blotting. With the successful replications of TGF-β induced EndMT, the results from silencing Nck with the presence of TGF-β presented the downregulation of both EC, CD31 and VE-Cad, and MC, vimentin, specific markers. The results suggest that Nck plays a critical role in TGF-β induced EndMT, while also provide a guide for future research of the signaling mechanisms modulated by Nck in TGF-β-stimulated cells. | en |
