Abstract:
:The effects of serum on inositol 1,4,5-trisphosphate (IP3) formation and Ca2+ mobilization in the human submandibular cell line A253 were studied. Exposure of A253 cells to fetal bovine serum (FBS) elicited a 3.3-fold increase in IP3 formation and a concentration-dependent transient increase in cytosolic free Ca2+ concentration ([Ca2+]i), which was similar in Ca2+-containing and Ca2+-free media. Newborn bovine serum (NBS), but not bovine serum albumin (BSA), induced a similar response. The Ca2+ release triggered by FBS was significantly (88%) reduced by the phospholipase C inhibitor U73122, indicating that Ca2+ release induced by FBS is through the PLC pathway. Pretreatment with the tyrosine kinase inhibitor genistein abolished the FBS- and NBS-induced Ca2+ release, suggesting that tyrosine kinase plays an important role in mediating the Ca2+ release. Pre-exposure to ATP or thapsigargin (TG) significantly reduced the FBS-induced [Ca2+]i increase, indicating that Ca2+ release caused by FBS is from the TG- or ATP-sensitive Ca2+ store. While FBS exposure elicited a large Ca2+ release, it reduced Ca2+ influx. Furthermore, FBS significantly inhibited the Ca2+ influx activated by the depletion of intracellular stores by ATP or TG. These results suggest that (1) serum elicits Ca2+ release from ATP- and TG-sensitive stores, which is mediated by IP3; (2) the serum-induced Ca2+ release may be modulated by a tyrosine kinase-associated process; and (3) serum strongly inhibits Ca2+ influxes including the store depletion-activated Ca2+ influx.
journal_name
J Cell Biochemjournal_title
Journal of cellular biochemistryauthors
Sun X,Mörk AC,Helmke RJ,Martinez JR,Zhang GHsubject
Has Abstractpub_date
1999-06-15 00:00:00pages
458-68issue
4eissn
0730-2312issn
1097-4644pii
10.1002/(SICI)1097-4644(19990615)73:4<458::AID-JCBjournal_volume
73pub_type
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