TGF-β inhibition of endothelial cell proliferation: alteration of EGF binding and EGF-induced growth-regulatory (competence) gene expression

K Takehara, EC LeRoy, GR Grotendorst - Cell, 1987 - cell.com
K Takehara, EC LeRoy, GR Grotendorst
Cell, 1987cell.com
Transforming growth factor-p (TGF-B) inhibits the growth of endothelial cells derived from
various sources, including human umbilical vein, bovine aorta, and rat heart. Long-term
exposure of rat heart endothelial cells to TGF-(3 also induces dramatic changes in
morphology that are characteristic of senescent cells. These changes are accompanied by a
decrease in the number of high-affinity receptors for epidermal growth factor (EGF), with
almost no change in total receptor number. Additionally, the EGF-induced expression of …
Summary
Transforming growth factor-p (TGF-B) inhibits the growth of endothelial cells derived from various sources, including human umbilical vein, bovine aorta, and rat heart. Long-term exposure of rat heart endothelial cells to TGF-(3 also induces dramatic changes in morphology that are characteristic of senescent cells. These changes are accompanied by a decrease in the number of high-affinity receptors for epidermal growth factor (EGF), with almost no change in total receptor number. Additionally, the EGF-induced expression of specific competence genes (c-myc, JE, KC) is decreased, whereas the induction of c-fos gene expression by EGF is unaltered by TGF-p treatment. These data suggest that growth Inhibitors such as TGF-f3 may act by altering the cell’s response to growth-stimulatory factors.
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