Expression Of Transforming Growth Factor-beta Receptors Research Articles

Regulation of transforming growth factor-beta receptor expression by hypoxia in vitro and in vivo

Regulation of transforming growth factor-beta receptor expression by hypoxia in vitro and in vivo

Vascular types I and II transforming growth factor-beta receptor expression: differential dependency on tyrosine kinases during induction by TGF- β

Recent evidence indicates that the type II transforming growth factor- β (TGF- β) receptor (T βRII) is a serine-threonine-tyrosine kinase. However, the significance of its tyrosine kinase is unclear. We investigated in vascular smooth muscle cells the effects of tyrosine kinase inhibition on the expression of TGF- β receptor types I (ALK-5) and II (T βRII) mRNA, induced by TGF- β 1. TGF- β 1 elevated ALK-5 mRNA levels 5-fold; essentially similar TGF- β 1-dependent elevations were observed with growth factors, PDGF-BB and FGF-2. The tyrosine kinase inhibitor genistein abolished these TGF- β 1 and growth factor responses. TGF- β 1 also elevated T βRII mRNA levels which were not inhibited by genistein. We conclude that tyrosine kinases participate in defining how cells respond to TGF- β.

Interferon-gamma induces high-affinity transforming growth factor-beta receptor expression on human corneal fibroblasts.

The effect of interferon-gamma (IFN-gamma) on the expression of transforming growth factor-beta (TGF-beta) receptors on cultured human corneal stromal fibroblasts was examined. Scatchard analysis of specific saturable TGF-beta 1 binding data indicated that corneal fibroblasts expressed TGF-beta receptors with an average association constant of 6 x 10 M-1, before and after IFN-gamma treatment. An additional population of higher affinity TGF-beta receptors, with an average association constant of 4 x 10(12) M-1, was demonstrated only on IFN-gamma-treated corneal fibroblasts Interferon-gamma may alter the response of corneal fibroblasts to transforming growth factor-betas by upregulating their higher affinity TGF-beta receptors. The induction of higher affinity TGF-beta receptors by an immune cytokine and an associated autocrine elevation of TGF-beta output by the corneal fibroblasts may be a transient compensatory mechanism that maintains the homeostasis of corneal optical competency through enhancement of corneal immunoseclusion.