title: Two types of store-operated Ca2+ channels with different activation modes and molecular origin in LNCaP human prostate cancer epithelial cells.
abstract: The one or more coupling mechanisms of store-operated channels (SOCs) to endoplasmic reticulum (ER) Ca2+ store depletion as well as the molecular identity of SOCs per se still remain a mystery. Here, we demonstrate the co-existence of two populations of molecular distinct endogenous SOCs in LNCaP prostate cancer epithelial cells, which are preferentially activated by either active inositol 1,4,5-trisphosphate (IP3)-mediated or passive thapsigargin-facilitated store depletion and have different ER store content sensitivity. The first population, called SOC(CC) (for "conformational coupling"), is characterized by preferential IP3 receptor-dependent mode of activation, as judged from sensitivity to cytoskeleton modifications, and dominant contribution of transient receptor potential (TRP) TRPC1 within it. The second one, called SOC(CIF) (for "calcium influx factor"), depends on Ca(2+)-independent phospholipase A2 for activation with probable CIF involvement and is mostly represented by TRPC4. The previously identified SOC constituent in LNCaP cells, TRPV6, seems to play equal role in both SOC populations. These results provide new insight into the nature of SOCs and their representation in the single cell type as well as permit reconciliation of current SOC activation hypotheses.
authors.affiliation: Laboratoire de Physiologie Cellulaire, INSERM EMI-0228, Université des Sciences et Technologies de Lille, Bat. SN3, 59655 Villeneuve d'Ascq, France.
authors.forename: Fabien
authors.initials: F
authors.lastname: Vanden Abeele
authors.forename: Loic
authors.initials: L
authors.lastname: Lemonnier
authors.forename: Stéphanie
authors.initials: S
authors.lastname: Thébault
authors.forename: Gilbert
authors.initials: G
authors.lastname: Lepage
authors.forename: Jan B
authors.initials: JB
authors.lastname: Parys
authors.forename: Yaroslav
authors.initials: Y
authors.lastname: Shuba
authors.forename: Roman
authors.initials: R
authors.lastname: Skryma
authors.forename: Natalia
authors.initials: N
authors.lastname: Prevarskaya
mesh_terms: D000199:Actins / Q000378:metabolism; D015153:Blotting, Western; D002118:Calcium / Q000737:chemistry / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism; D020013:Calcium Signaling; D045744:Cell Line, Tumor; D003599:Cytoskeleton / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004594:Electrophysiology; D004721:Endoplasmic Reticulum / Q000378:metabolism; D004847:Epithelial Cells / Q000378:metabolism; D006801:Humans; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism; D053496:Inositol 1,4,5-Trisphosphate Receptors; D008297:Male; D008856:Microscopy, Fluorescence; D008954:Models, Biological; D016376:Oligonucleotides, Antisense / Q000737:chemistry / Q000494:pharmacology; D011471:Prostatic Neoplasms / Q000378:metabolism*; D011487:Protein Conformation; D020033:Protein Isoforms; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D015398:Signal Transduction; D050916:TRPV Cation Channels; D019284:Thapsigargin / Q000494:pharmacology; D013997:Time Factors
chemical_list: D000199:Actins; D015220:Calcium Channels; C506926:ITPR1 protein, human; D053496:Inositol 1,4,5-Trisphosphate Receptors; D016376:Oligonucleotides, Antisense; D020033:Protein Isoforms; D018160:Receptors, Cytoplasmic and Nuclear; D050916:TRPV Cation Channels; C120776:TRPV6 channel; D019284:Thapsigargin; D015544:Inositol 1,4,5-Trisphosphate; D002118:Calcium