title: Distinct mechanisms of [Ca2+]i oscillations in HSY and HSG cells: role of Ca2+ influx and internal Ca2+ store recycling.
abstract: This study examined [Ca2+]i oscillations in the human salivary gland cell lines, HSY and HSG. Relatively low concentrations of carbachol (CCh) induced oscillatory, and higher [CCh] induced sustained, steady-state increases in [Ca2+]i and KCa currents in both cell types. Low IP3, but not thapsigargin (Tg), induced [Ca2+]i oscillations, whereas Tg blocked CCh-stimulated [Ca2+]i oscillations in both cell types. Unlike in HSG cells, removal of extracellular Ca2+ from HSY cells (i) did not affect CCh-stimulated [Ca2+]i oscillations or internal Ca2+ store refill, and (ii) converted high [CCh]-induced steady-state increase in [Ca2+]i into oscillations. CCh- or thapsigargin-induced Ca2+ influx was higher in HSY, than in HSG, cells. Importantly, HSY cells displayed relatively higher levels of sarcoendoplasmic reticulum Ca2+ pump (SERCA) and inositoltrisphosphate receptors (IP3Rs) than HSG cells. These data demonstrate that [Ca2+]i oscillations in both HSY and HSG cells are primarily determined by the uptake of Ca2+ from, and release of Ca2+ into, the cytosol by the SERCA and IP3R activities, respectively. In HSY cells, Ca2+ influx does not acutely contribute to this process, although it determines the steady-state increase in [Ca2+]i. In HSG cells, [Ca2+]i oscillations directly depend on Ca2+ influx; Ca2+ coming into the cell is rapidly taken up into the store and then released into the cytosol. We suggest that the differences in the mechanism of [Ca2+]i oscillations HSY and HSG cells is related to their respective abilities to recycle internal Ca2+ stores.
authors: Secretory Physiology Section, Gene Therapy and Therapeutics Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892, USA.
authors: X
authors: X
authors: Liu
authors: D
authors: D
authors: Liao
authors: I S
authors: IS
authors: Ambudkar
mesh_terms: D015153:Blotting, Western; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D015220:Calcium Channels / Q000378:metabolism; D020013:Calcium Signaling / Q000187:drug effects; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D002217:Carbachol / Q000494:pharmacology; D002460:Cell Line; D004553:Electric Conductivity; D004591:Electrophoresis, Polyacrylamide Gel; D006801:Humans; D053496:Inositol 1,4,5-Trisphosphate Receptors; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D012469:Salivary Glands / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D019284:Thapsigargin / Q000494:pharmacology
chemical_list: D015220:Calcium Channels; C506926:ITPR1 protein, human; D053496:Inositol 1,4,5-Trisphosphate Receptors; D018160:Receptors, Cytoplasmic and Nuclear; D019284:Thapsigargin; D002217:Carbachol; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D000252:Calcium-Transporting ATPases; D011188:Potassium; D002118:Calcium