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Ciglitizone inhibits cell proliferation in human uterine leiomyoma via activation of store-operated Ca2+ channels

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Author(s)
Byoung Ywong KimChi-Heum ChoDae-Kyu SongKyo-Cheol MunSeong-Il SuhSang-Pyo KimDong-Hoon ShinByeong-Churl JangTaeg Kyu KwonSoon-Do ChaInsoo BaeJae Hoon Bae
Keimyung Author(s)
Song, Dae KyuBae, Jae HoonCho, Chi HeumCha, Soon DoMun, Kyo CheolSuh, Seong IlKim, Sang PyoJang, Byeong ChurlShin, Dong HoonKwon, Taeg Kyu
Department
Dept. of Physiology (생리학)
Dept. of Obstetrics & Gynecology (산부인과학)
Dept. of Biochemistry (생화학)
Dept. of Microbiology (미생물학)
Dept. of Pathology (병리학)
Dept. of Molecular Medicine (분자의학)
Dept. of Preventive Medicine (예방의학)
Dept. of Immunology (면역학)
Journal Title
American Journal of Physiology : Cell Physiology
Issued Date
2005
Volume
288
Issue
2
Abstract
This study investigated the acute effects of a peroxisome proliferator-activated receptor (PPAR)-γ ligand, ciglitizone, on cell proliferation and intracellular Ca2+ signaling in human normal myometrium and uterine leiomyoma. Changes in intracellular Ca2+ concentration ([Ca2+]i) were measured with fura-2 AM, and cellular viabilities were determined by viable cell count and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide reduction assay. Ciglitizone (100 μM) induced greater inhibition of cell proliferation in uterine leiomyoma than in myometrium. Ciglitizone also dose-dependently increased [Ca2+]i in both myometrium and uterine leiomyoma; these [Ca2+]i increases were inhibited by PPAR-γ antagonists and raloxifene. Ciglitizone-induced [Ca2+]i increase showed only an initial peak in normal myometrial cells, whereas in uterine leiomyoma there was a second sustained [Ca2+]i increase as well. The initial [Ca2+]i increase in both myometrium and uterine leiomyoma resulted from the release of Ca2+ by the sarcoplasmic reticulum via activation of ryanodine receptors. The second [Ca2+]i increase was observed only in uterine leiomyoma because of a Ca2+ influx via an activation of store-operated Ca2+ channels (SOCCs). Cell proliferation was inhibited and secondary [Ca2+]i increase in uterine leiomyoma was attenuated by cotreatment of ciglitizone with a SOCC blocker, lanthanum. The results suggest that ciglitizone inhibits cell proliferation and increases [Ca2+]i through the activation of SOCCs, especially in human uterine leiomyoma.
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