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ENDOCRINE AND REPRODUCTIVE

Role of Protein Kinase C-Ras-MAPK p44/42 in Ethanol and Transforming Growth Factor-3-Induced Basic Fibroblast Growth Factor Release from Folliculostellate Cells

Endocrinology Program and Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, New Jersey

In the present study, we determined the interactive effects of ethanol and transforming growth factor -3 (TGF-3) on basic fibroblast growth factor (bFGF) release from folliculostellate (FS) cells and the role of the mitogen-activated protein kinase (MAPK) pathway in this interaction. We found that TGF-3 and ethanol alone increased release of bFGF from FS cells, but together they showed markedly increased levels of bFGF compared with the individual effect. Ethanol and TGF-3 alone moderately increased activation of MAPK p44/42, but together they produced marked activation of MAPK p44/42. TGF-3 alone increased the activation of smad2. Ethanol did not activate smad2 or alter TGF-3 activation of smad2. Pretreatment of FS cells with a mitogen-activated protein kinase kinase 1/2 inhibitor or with a protein kinase C (PKC) inhibitor suppressed the TGF-3 and ethanol actions on MAPK p44/42 activation and bFGF release. Ethanol and TGF-3, either alone or in combination, increased the levels of active Ras. Furthermore, the MAPK p44/42 activation by TGF-3 and ethanol was blocked by overexpression of Ras N17, a dominant negative mutant of Ras p21. These data suggest that the PKC-activated Ras-dependent MAPK p44/42 pathway is involved in the cross talk between TGF-3 and ethanol to increase bFGF release from FS cells.

Address correspondence to: Dr. Dipak K. Sarkar, 84 Lipman Dr., New Brunswick, NJ 08901. E-mail: sarkar{at}aesop.rutgers.edu

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