ISSN:
1432-2013
Keywords:
Key words Ca2+ entry
;
Mn2+ entry
;
Protein kinase
;
Staurosporine
;
K-252a
;
Salivary glands
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Divalent cation (Ca2+ and Mn2+) influx, stimulated by internal Ca2+ store depletion, into rat parotid acinar cells is inhibited by conditions which increase protein phosphorylation [T. Sakai and I.S. Ambudkar (1996) Am J Physiol 271:C284–C294]. The present study examines the involvement of this protein phosphorylation and Ca2+ in the store-dependent inactivation of divalent cation entry. Internal Ca2+ store depletion, achieved by incubation (30 min) of cells in nominally Ca2+-free medium containing either carbachol or thapsigargin, stimulated Ca2+, and Mn2+, influx into cells. In either case, inclusion of 1.5 mM Ca2+ for the last 5 min of incubation resulted in a decrease in Ca2+ (33–41%) and Mn2+ (50%) influx, which could not be accounted for by internal Ca2+ store refill. The inhibition was prevented when internal-store-depleted cells were treated (prior to incubation with Ca2+) with either staurosporine or K-252a, but not with H-7 or KN-93. Refilling of internal Ca2+ store(s) in carbachol-treated cells (incubation with Ca2++atropine) induced complete inhibition of divalent cation influx, which was not prevented by treatment with protein kinase inhibitors. These data suggest the staurosporine-sensitive (and K-252a-sensitive) protein phosphorylation is not involved in Ca2+-store-refilling-dependent inactivation of Ca2+ influx but mediates a Ca2+-dependent feedback modulation of divalent cation influx in rat parotid gland acinar cells.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s004240050301
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