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Am J Physiol Cell Physiol (February 2, 2005). doi:10.1152/ajpcell.00370.2004
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Submitted on July 29, 2004
Accepted on January 27, 2005

{beta}-Adrenergic Responsive Activation of Extracellular Signal-regulated Protein Kinases in Salivary Cells: Role of Epidermal Growth Factor Receptor and cAMP

Chih-Ko Yeh1, Paramita M. Ghosh2, Howard Dang3, Qun Liu4, Alan L. Lin5, Bin-Xian Zhang6, and Michael S. Katz7*

1 Geriatric Research, Education & Clinical Center, South Texas Veterans Health Care System, San Antonio, Texas, USA; Dental Diagnostic Science, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA; Community Dentistry, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA
2 Surgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA
3 Community Dentistry, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA
4 Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA
5 Dental Diagnostic Science, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA
6 Research Service, South Texas Veterans Health Care System, San Antonio, Texas, USA; Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA
7 Geriatric Research, Education & Clinical Center, South Texas Veterans Health Care System, San Antonio, Texas, USA; Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA

* To whom correspondence should be addressed. E-mail: katz{at}uthscsa.edu.

ABSTRACT The {beta}-adrenergic receptor agonist isoproterenol exerts growth-promoting effects on salivary glands. In this study activation of extracellular signal-regulated kinases (ERKs), members of the mitogen activated protein kinase family, by isoproterenol was examined in a human salivary gland cell line (HSY). Immunoblot analysis indicated that isoproterenol (10-5 M) induced transient activation of ERK1/2 (4.4 fold relative to basal at 10 min) similar to that caused by epidermal growth factor (EGF) (6.7 fold). Isoproterenol, like EGF, also induced phosphorylation of the EGF receptor. However, inhibition of EGF receptor phosphorylation by the tyrphostin AG1478 only partially attenuated isoproterenol induced ERK phosphorylation, while EGF responsive ERK activation was completely blocked. The Gi inhibitor pertussis toxin also caused partial inhibition of isoproterenol stimulated ERK activation. The cAMP analog cpt-cAMP and the cAMP elevating agents IBMX and cholera toxin produced transient ERK1/2 activation, similar to the effect of isoproterenol, in HSY cells. The stimulatory effects of isoproterenol and cAMP on ERK phosphorylation were not reduced by the protein kinase A (PKA) inhibitor H-89, whereas the Src-family inhibitor PP2 and transfection of a dominant negative Src construct diminished isoproterenol induced ERK activation. Isoproterenol induced marked overexpression of the cell-growth related adhesion molecule CD44, and this effect of isoproterenol was abolished by the ERK pathway inhibitor PD98059. In summary, we show a dual mechanism of isoproterenol induced ERK phosphorylation in HSY cells - one pathway mediated by EGF receptor transactivation and the other by an EGF receptor-independent pathway possibly mediated by cAMP. Our results also suggest that isoproterenol induced growth of salivary tissue may involve ERK mediated CD44 expression.




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