title: Distinct Ca(2+)-permeable cation currents are activated by internal Ca(2+)-store depletion in RBL-2H3 cells and human salivary gland cells, HSG and HSY.
abstract: Store-operated Ca(2+) influx, suggested to be mediated via store-operated cation channel (SOC), is present in all cells. The molecular basis of SOC, and possible heterogeneity of these channels, are still a matter of controversy. Here we have compared the properties of SOC currents ( I(SOC)) in human submandibular glands cells (HSG) and human parotid gland cells (HSY) with I(CRAC) (Ca(2+) release-activated Ca(2+) current) in RBL cells. Internal Ca(2+) store-depletion with IP(3) or thapsigargin activated cation channels in all three cell types. 1 muM Gd(3+) blocked channel activity in all cells. Washout of Gd(3+) induced partial recovery in HSY and HSG but not RBL cells. 2-APB reversibly inhibited the channels in all cells. I(CRAC )in RBL cells displayed strong inward rectification with E(rev)(Ca) = >+90 mV and E(rev) (Na) = +60 mV. I(SOC) in HSG cells showed weaker rectification with E(rev)(Ca) = +25 mV and E(rev)(Na) = +10 mV. HSY cells displayed a linear current with E(rev) = +5 mV, which was similar in Ca(2+)- or Na(+)-containing medium. pCa/ pNa was >500, 40, and 4.6 while pCs / pNa was 0.1,1, and 1.3, for RBL, HSG, and HSY cells, respectively. Evidence for anomalous mole fraction behavior of Ca(2+)/Na(+) permeation was obtained with RBL and HSG cells but not HSY cells. Additionally, channel inactivation with Ca(2+) + Na(+) or Na(+) in the bath was different in the three cell types. In aggregate, these data demonstrate that distinct store-dependent cation currents are stimulated in RBL, HSG, and HSY cells. Importantly, these data suggest a molecular heterogeneity, and possibly cell-specific differences in the function, of these channels.
authors.affiliation: Secretory Physiology Section, Gene Therapy and Therapeutics Branch, National Institutes of Dental and Craniofacial Research, NIH, DHHS, Bethesda, MD 20892, USA.
authors.forename: X
authors.initials: X
authors.lastname: Liu
authors.forename: K
authors.initials: K
authors.lastname: Groschner
authors.forename: I S
authors.initials: IS
authors.lastname: Ambudkar
mesh_terms: D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism*; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology; D002412:Cations / Q000378:metabolism; D002460:Cell Line; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006801:Humans; D015544:Inositol 1,4,5-Trisphosphate / Q000494:pharmacology; D015640:Ion Channel Gating / Q000187:drug effects; D008564:Membrane Potentials / Q000187:drug effects; D010306:Parotid Gland / Q000166:cytology / Q000502:physiology*; D018408:Patch-Clamp Techniques; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D013363:Submandibular Gland / Q000166:cytology / Q000502:physiology*; D019284:Thapsigargin / Q000494:pharmacology
chemical_list: D015220:Calcium Channels; D002412:Cations; D004791:Enzyme Inhibitors; D002104:Cadmium; D019284:Thapsigargin; D015544:Inositol 1,4,5-Trisphosphate; D002118:Calcium