title: Store-mediated calcium entry in pleural mesothelial cells.
abstract: Store-mediated Ca2+ entry is thought as the main pathway for Ca2+ influx in non-excitable cells. Although a role for the actin cytoskeleton in store-mediated Ca2+ entry has been proposed in some cell types, the role of actin cytoskeleton in store-mediated Ca2+ entry is still a controversy. To address this question, the effects of cytoskeletal modifiers on store-mediated Ca2+ entry in pleural mesothelial cells were examined. Thapsigargin (1 microM) induced a sufficient signal for the activation of store-mediated Ca2+ entry in pleural mesothelial cells. In the absence of extracellular Ca2+, thapsigargin induced only a transient elevation of [Ca2+]i. Moreover, re-addition of Ca2+ increased the elevation of [Ca2+]i. Passive elevations in [Ca2+]i without thapsigargin, which is induced from Ca2+ containing solution switch to Ca2+ free solution and re-add Ca2+ containing solution, were not observed in pleural mesothelial cells. Thapsigargin-induced Ca2+ entry was still present after nifedipine (1 microM) treatment. However, SKF96365 (1 microM) blocked thapsigargin-induced Ca2+ entry. Mycalolide B (1 microM) completely disrupts actin cytoskeleton in pleural mesothelial cells, but thapsigargin-induced store-mediated Ca2+ entry was preserved. Jasplakinolide (3 microM) prevented thapsigargin-induced store-mediated Ca2+ entry. These results suggest that store-mediated Ca2+ entry in pleural mesothelial cells may be mediated by a recently proposed secretion-like coupling model for store-mediated Ca2+ entry.
authors.affiliation: Department of Comparative Pathophysiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan. akuwam@mail.ecc.u-tokyo.ac.jp
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Kuwahara
authors.forename: Maki
authors.initials: M
authors.lastname: Kuwahara
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D048430:Cell Shape / Q000187:drug effects; D002478:Cells, Cultured; D015638:Cytochalasin D / Q000494:pharmacology; D003599:Cytoskeleton / Q000378:metabolism; D047630:Depsipeptides / Q000494:pharmacology; D004847:Epithelial Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D007093:Imidazoles / Q000494:pharmacology; D008387:Marine Toxins; D018613:Microscopy, Confocal; D009543:Nifedipine / Q000494:pharmacology; D010080:Oxazoles / Q000494:pharmacology; D010994:Pleura / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D019284:Thapsigargin / Q000494:pharmacology
chemical_list: D000199:Actins; D047630:Depsipeptides; D007093:Imidazoles; D008387:Marine Toxins; D010080:Oxazoles; C057531:jasplakinolide; C080978:mycalolide B; D015638:Cytochalasin D; D019284:Thapsigargin; C063159:1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole; D009543:Nifedipine; D002118:Calcium