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J. Biol. Chem., Vol. 277, Issue 50, 48165-48171, December 13, 2002

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Epidermal Growth Factor-induced Depletion of the Intracellular Ca²⁺ Store Fails to Activate Capacitative Ca²⁺ Entry in a Human Salivary Cell Line^*

Bin-Xian Zhang^§, Xiuye Ma^¶, Chih-Ko Yeh^**, Meyer D. Lifschitz^§, Michael X. Zhu, and Michael S. Katz^§

From the  Medical Research Service and  Geriatric Research, Education and Clinical Center, South Texas Veterans Health Care System, Audie L. Murphy Division, San Antonio, Texas 78229, Departments of ^§ Medicine, ^¶ Biochemistry, and ^** Dental Diagnostic Science, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229, and  Neurobiotechnology Center and Department of Neuroscience, Ohio State University, Columbus, Ohio 43210

Epidermal growth factor (EGF) is a multifunctional factor known to influence proliferation and function of a variety of cells. The actions of EGF are mediated by EGF receptor tyrosine kinase pathways, including stimulation of phospholipase C and mobilization of intracellular Ca²⁺ ([Ca²⁺]_i). Generally, agonist-mediated Ca²⁺ mobilization involves both Ca²⁺ release from internal stores and Ca²⁺ influx activated by store depletion (i.e. capacitative or store-operated Ca²⁺ influx). However, the role of capacitative Ca²⁺ entry in EGF-mediated Ca²⁺ mobilization is still largely unknown. In this study, we compared [Ca²⁺]_i signals elicited by EGF with those induced by agents (the muscarinic receptor agonist carbachol and thapsigargin (Tg)) known to activate capacitative Ca²⁺ entry. Unlike carbachol and Tg, EGF (5 nM) elicited a transient [Ca²⁺]_i signal without a plateau phase in the presence of extracellular Ca²⁺ and also failed to accelerate Mn²⁺ entry. Repletion of extracellular Ca²⁺ to cells stimulated with EGF in the absence of Ca²⁺ elicited an increase in [Ca²⁺]_i, indicating that EGF indeed stimulates Ca²⁺ influx. However, the influx was activated at lower EGF concentrations than those required to stimulate Ca²⁺ release. Interestingly, the phospholipase C inhibitor U73122 completely inhibited Ca²⁺ release induced by both EGF and carbachol and also reduced Ca²⁺ influx responsive to carbachol but had no effect on Ca²⁺ influx induced by EGF. EGF-induced Ca²⁺ influx was potentiated by low concentrations (<5 ng/ml) of oligomycin, a mitochondrial inhibitor that blocks capacitative Ca²⁺ influx in other systems. Transient expression of the hTRPC3 protein enhanced Ca²⁺ influx responsive to carbachol but did not increase EGF-activated Ca²⁺ influx. Both EGF and carbachol depleted internal Ca²⁺ stores. Our results demonstrate that EGF-induced Ca²⁺ release from internal stores does not activate capacitative Ca²⁺ influx. Rather, EGF stimulates Ca²⁺ influx via a mechanism distinct from capacitative Ca²⁺ influx induced by carbachol and Tg.

§§ To whom correspondence should be addressed: 7400 Merton Minter Blvd., San Antonio, TX 78229-4404. Tel.: 210-617-5197; Fax: 210-617-5312; E-mail: katz@uthscsa.edu

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