scholarly journals An aldose reductase inhibitor prevents glucose-induced increase in transforming growth factor-? and protein kinase C activity in cultured human mesangial cells

Diabetologia ◽  
1998 ◽  
Vol 41 (3) ◽  
pp. 362-364 ◽  
Author(s):  
H. Ishii ◽  
H. Tada ◽  
S. Isogai
Keyword(s):  
Protein Kinase C ◽  
Growth Factor ◽  
Protein Kinase ◽  
Reductase Inhibitor ◽  
Transforming Growth Factor ◽  
Mesangial Cells ◽  
Aldose Reductase Inhibitor ◽  
Human Mesangial Cells ◽  
Kinase C ◽  
Protein Kinase C Activity

Activation of Glomerular Mesangial Cells by Hepatocyte Growth Factor Through Tyrosine Kinase and Protein Kinase C

1998 ◽  
Vol 55 (2) ◽  
pp. 227-234 ◽  
Author(s):  
Nicholas J Laping ◽  
Barbara A Olson ◽  
Robin E DeWolf ◽  
Christine R Albrightson ◽  
Todd Fredrickson ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Growth Factor ◽  
Protein Kinase ◽  
Hepatocyte Growth Factor ◽  
Tyrosine Kinase ◽  
Mesangial Cells ◽  
Glomerular Mesangial Cells ◽  
Kinase C ◽  
Hepatocyte Growth

scholarly journals Epidermal growth factor stimulation of stromelysin mRNA in rat fibroblasts requires induction of proto-oncogenes c-fos and c-jun and activation of protein kinase C.

1990 ◽  
Vol 10 (8) ◽  
pp. 4284-4293 ◽  
Author(s):  
S E McDonnell ◽  
L D Kerr ◽  
L M Matrisian
Keyword(s):  
Protein Kinase C ◽  
Growth Factor ◽  
Protein Kinase ◽  
Epidermal Growth Factor ◽  
Kinase Activation ◽  
Kinase C ◽  
Protein Kinase C Activity ◽  
Epidermal Growth ◽  
Rat Fibroblasts ◽  
Stimulation Of

Stromelysin (transin) is a secreted metalloprotease that is transcriptionally induced by a variety of growth factors and oncogenes. We examined the necessity of specific secondary (protein kinase C) and tertiary (c-fos and c-jun protein products) messengers in the transactivation of stromelysin gene expression by epidermal growth factor (EGF). Rat-1 fibroblasts exposed to antisense c-fos DNA or RNA demonstrated that c-fos expression was necessary for complete EGF induction of stromelysin expression. Similar results demonstrating the necessity of c-jun protein in the EGF induction of stromelysin were obtained. We also demonstrated that protein kinase C activation is required for the EGF induction of stromelysin, since phorbol ester desensitization of C kinase proteins abolished the ability of EGF to induce stromelysin mRNA, protein, and promoter activity. In reconstitution experiments, neither c-fos, c-jun, nor C kinase activation alone induced significant stromelysin expression. Overexpression of c-fos and c-jun was able to induce stromelysin to a level similar to that of the growth factor, and stimulation of protein kinase C activity augmented this induction. The data suggest that the EGF induction of stromelysin in rat fibroblasts procedes through a pathway involving c-fos, c-jun, and protein kinase C.

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