Activation of protein kinase-C differentially regulates insulin-like growth factor-I and basic fibroblast growth factor messenger RNA levels

1992 ◽  
Vol 6 (5) ◽  
pp. 741-752 ◽  
Author(s):  
W. L. Lowe
Keyword(s):  
Protein Kinase C ◽  
Growth Factor ◽  
Protein Kinase ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Messenger Rna ◽  
Insulin Like Growth Factor ◽  
Fibroblast Growth ◽  
Factor I ◽  
Kinase C

scholarly journals A growth factor-repressible gene associated with protein kinase C-mediated inhibition of adipocyte differentiation.

1988 ◽  
Vol 107 (1) ◽  
pp. 279-286 ◽  
Author(s):  
M Navre ◽  
G M Ringold
Keyword(s):  
Protein Kinase C ◽  
Growth Factor ◽  
Protein Kinase ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Phorbol Esters ◽  
Adipocyte Differentiation ◽  
Fibroblast Growth ◽  
Kinase C

The conversion of determined adipoblasts to fully differentiated adipocytes requires appropriate environmental conditions. A strict dependence on cell confluence and a facilitation by glucocorticoid hormones have previously been described. We have found that agents that are capable of activating protein kinase C, such as basic fibroblast growth factor and phorbol esters, inhibit the differentiation of the adipogenic cell line TA1 without stimulating cell growth. Here we describe the sequence and characterization of a cDNA (clone 5) that detects an RNA, the expression of which is enhanced by glucocorticoids and increasing cell density. In contrast, activators of protein kinase C including basic fibroblast growth factor, phorbol esters, and synthetic diacylglycerols inhibit clone 5 gene expression. It appears that clone 5 expression is closely linked to environmental and hormonal factors that promote the differentiation of adipogenic cells.

Stimulatory Effect of Basic Fibroblast Growth Factor on Induction of Heat Shock Protein 27 in Osteoblasts: Role of Protein Kinase C

2001 ◽  
Vol 388 (2) ◽  
pp. 237-242 ◽  
Author(s):  
Osamu Kozawa ◽  
Masayuki Niwa ◽  
Hiroyuki Matsuno ◽  
Akira Ishisaki ◽  
Kanefusa Kato ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Growth Factor ◽  
Heat Shock ◽  
Protein Kinase ◽  
Heat Shock Protein ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
Kinase C

scholarly journals Involvement of Protein Kinase C-Dependent Mitogen-Activated Protein Kinase p44/42 Signaling Pathway for Cross-Talk between Estradiol and Transforming Growth Factor-β3 in Increasing Basic Fibroblast Growth Factor in Folliculostellate Cells

Endocrinology ◽  
2004 ◽  
Vol 145 (2) ◽  
pp. 706-715 ◽  
Author(s):  
Kirti Chaturvedi ◽  
Dipak K. Sarkar
Keyword(s):  
Protein Kinase C ◽  
Growth Factor ◽  
Protein Kinase ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Cross Talk ◽  
Mapk Pathway ◽  
Dominant Negative Mutant ◽  
Fibroblast Growth ◽  
Kinase C

Abstract We have recently shown that TGF-β3, in the presence of estradiol, increases the release of basic fibroblast growth factor (bFGF) from folliculostellate (FS) cells in the pituitary. We determined the interactive effects of TGF-β3 and estradiol on bFGF production and release from FS cells, and the role of the MAPK pathway in TGF-β3 and estradiol interaction. We found that TGF-β3 and estradiol alone moderately increased cell content and release of bFGF from FS cells; but together, they markedly increased the peptide. Estradiol and TGF-β3 alone moderately activated MAPK p44/42; together they produced marked activation of MAPK p44/42. Pretreatment of FS cells with an MAPK kinase 1/2 inhibitor or with protein kinase C inhibitors suppressed the activation of MAPK p44/42, bFGF release, and protein level increases, all of which were induced by TGF-β3 and estradiol. Estradiol and TGF-β3, either alone or in combination, increased the levels of active Ras. Furthermore, bFGF induction by TGF-β3 and estradiol was blocked by overexpression of Ras N17, a dominant negative mutant of Ras p21. Estrogen receptor blocker ICI 182,780 failed to prevent estrogen’s and TGF-β3’s effects on bFGF. These data suggest that an estradiol receptor-independent protein kinase C- activated Ras-dependent MAPK pathway is involved in the cross-talk between TGF-β3 and estradiol to increase bFGF production and/or release from FS cells.

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