Differential modulation of vascular cell integrin and extracellular matrix expression in vitro by TGF‐β1 correlates with reciprocal effects on cell migration+

CT Basson, O Kocher, MD Basson… - Journal of cellular …, 1992 - Wiley Online Library
CT Basson, O Kocher, MD Basson, A Asis, JA Madri
Journal of cellular physiology, 1992Wiley Online Library
In vitro, BAEC and BASMC migratory phenotypes are known to be reciprocally modulated by
both soluble factors and extracellular matrix proteins. In addition, integrin matrix receptors
mediate endothelial and smooth muscle cell attachment and migration. To further elucidate
these phenomena, we studied the effects of TGF‐β1 on intergin expression by vascular
BASMC and BAEC in tissue culture. TGF‐β1 upregulated mRNA levels and surface pools of
BASMC β3 integrin classes without modulating β1 integrin mRNA levels or expression of β1 …
Abstract
In vitro, BAEC and BASMC migratory phenotypes are known to be reciprocally modulated by both soluble factors and extracellular matrix proteins. In addition, integrin matrix receptors mediate endothelial and smooth muscle cell attachment and migration. To further elucidate these phenomena, we studied the effects of TGF‐β1 on intergin expression by vascular BASMC and BAEC in tissue culture. TGF‐β1 upregulated mRNA levels and surface pools of BASMC β3 integrin classes without modulating β1 integrin mRNA levels or expression of β1 integrin organization. In contrast to its effect on BASMC, TGF‐β1 increased BAFC mRNA levels and surface expression of β1 and β3 integrins without altering their organization. Conversely, extracellular matrix components (fibronectin, laminin, and fibrinogen) organized cell surface integrins in both BASMC and BAEC without affecting the size of their cell surface pools. These data are consistent with the hypothesis that SMC and EC behavior in neointimal lesions may modulated in part, through a coordination of soluble factor and extracellular matrix protein regulation of integrin surface expression and organization. © 1992 Wiley‐Liss, Inc.
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