Induction of nerve growth factor and basic fibroblast growth factor mRNA following clenbuterol: Contrasting anatomical and cellular localization

1995 ◽  
Vol 132 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Valerie Y. Hayes ◽  
Paul J. Isackson ◽  
Michele Fabrazzo ◽  
Paolo Follesa ◽  
Italo Mocchetti
1990 ◽  
Vol 10 (4) ◽  
pp. 1556-1563 ◽  
Author(s):  
T M Thomson ◽  
S H Green ◽  
R J Trotta ◽  
D E Burstein ◽  
A Pellicer

A cell line was generated from U7 cells (a subline of PC12 rat pheochromocytoma cells) that contains a stably integrated transforming mouse N-ras (Lys-61) gene under the control of the long terminal repeat from mouse mammary tumor virus. Such cells, designated UR61, undergo neuronal differentiation upon exposure to nanomolar concentrations of dexamethasone, as a consequence of expression of the activated N-ras gene (I. Guerrero, A. Pellicer, and D.E. Burstein, Biochem, Biophys. Res. Commun. 150:1185-1192, 1988). Exposure of UR61 cells to either nerve growth factor (NGF) or basic fibroblast growth factor (bFGF) results in a marked induction of c-fos RNA, with kinetics paralleling those of NGF- or bFGF-induced expression of c-fos RNA in PC12 cells. Dexamethasone-induced expression of activated N-ras p21 results in blocking of c-fos RNA induction by NGF or bFGF in a time-dependent manner. Activated N-ras p21-mediated inhibition of c-fos RNA induction in UR61 cells is selective for NGF and bFGF and is not due to selective degradation of c-fos RNA. Normal and transforming N-ras can trans activate the chloramphenicol acetyltransferase gene linked to mouse c-fos regulatory sequences when transient expression assays are performed. Our observations suggest that N-ras p21 selectively interacts with pathways involved in induction of c-fos expression which initiate at the receptors for NGF and bFGF.


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