Modulation of the Endothelial Phenotype by Transforming Growth Factor-β2 and Nck Signaling
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The development of solid tumors and atherosclerosis requires neovascularization. In contrast to blood vessels of healthy organs, blood vessels associated with atherosclerosis and tumors are poorly organized and leaky. However, it is poorly understood how microenvironmental factors modulate molecular mechanisms underlying the abnormal vascular phenotype. The objective in this project is to determine cellular changes elicited by transforming growth factor-β2 (TGF-β2) and the Nck adaptors in the transition of endothelial sheets from a stable/cohesive to a loosely organized, permeable phenotype. It is hypothesized that the Nck adaptors link heightened matrix stiffness and TGF-β2 signaling thereby inducing cytoskeletal changes underlying the tumor-associated endothelial phenotype. Cell culture experiments coupled with immunofluorescence labeling indicate change in cell morphology and patterns of protein expression/subcellular distribution when TGF-β2-treated cells were compared with control endothelial cells. Preliminary results indicate the Nck modulates TGF-beta-induced changes in cell morphology. These results suggest that the TGF-β2 signaling pathway and/or the silencing of the Nck could be targeted to prevent Endothelial to Mesenchymal Transition (EndMT) and the abnormal vasculature in atherosclerosis.
SubjectTGF-β2-treated cells (TGF-β2)
Endothelial to Mesenchymal Transition (EndMT)
Human Umbilical Vein Endothelial Cells
Polyethylene glycol hydrogels
smooth muscle 22
Vascular Endothelial Growth Factor
silencing Nck adaptor proteins
Pham, Thao-Nguyen T (2020). Modulation of the Endothelial Phenotype by Transforming Growth Factor-β2 and Nck Signaling. Undergraduate Research Scholars Program. Available electronically from
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