Mammalian ciliary-body epithelial cells in culture produce transforming growth factor-beta

1991 ◽  
Vol 229 (1) ◽  
pp. 84-87 ◽  
Author(s):  
Horst Helbig ◽  
Karen L. Kittredge ◽  
Miguel Coca-Prados ◽  
Janet Davis ◽  
Alan G. Palestine ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Transforming Growth Factor Beta ◽  
Ciliary Body ◽  
Transforming Growth Factor ◽  
Cells In Culture ◽  
Growth Factor Beta

Interaction of epidermal growth factor and transforming growth factor beta in human prostatic epithelial cells in culture

The Prostate ◽  
1992 ◽  
Vol 21 (2) ◽  
pp. 133-143 ◽  
Author(s):  
Debra M. Sutkowski ◽  
Chau-Jye Fong ◽  
Julia A. Sensibar ◽  
Alfred W. Rademaker ◽  
Edward R. Sherwood ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Cells In Culture ◽  
Epidermal Growth ◽  
Growth Factor Beta

Transforming growth factor-beta inhibits phosphate transport in renal epithelial cells

1993 ◽  
Vol 264 (4) ◽  
pp. F623-F628 ◽  
Author(s):  
F. Law ◽  
R. Rizzoli ◽  
J. P. Bonjour
Keyword(s):  
Growth Factor ◽  
Protein Kinase ◽  
Epithelial Cells ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Tgf Beta ◽  
Renal Epithelial Cells ◽  
Pi Transport ◽  
Sodium Dependent ◽  
Growth Factor Beta

The effect(s) of transforming growth factor-beta (TGF-beta) on Pi transport was investigated in confluent opossum kidney (OK) epithelial cells. TGF-beta induced a time- and concentration-dependent decrease in the initial rate of sodium-dependent Pi, but not alanine, transport. This selective inhibitory effect on Pi transport was largely reversible and was not associated with a rise in adenosine 3',5'-cyclic monophosphate production. The reduction in Pi uptake was also independent of changes in extracellular calcium concentrations and prostaglandin synthesis. TGF-beta-mediated Pi transport inhibition appeared to involve neither pertussis toxin-sensitive G protein(s) nor augmented protein kinase C activity. However, the probable role of a serine/threonine protein kinase in signal transduction was supported by the considerable attenuation of TGF-beta effect by H-7. Furthermore, the TGF-beta-induced Pi transport reduction was blunted by cycloheximide and abolished by actinomycin D. In conclusion, TGF-beta selectively inhibits the activity of the sodium-dependent Pi transport system present in the apical membrane of renal epithelial cells. This action appears to be exerted via an unprecedented inhibitory pathway that might involve a serine/threonine protein kinase and alterations in the transcriptional and translational processes.

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