Purinoceptor-Mediated Calcium Mobilization and Cellular Proliferation in Cultured Bovine Corneal Endothelial Cells.

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  • Ho Cha Seok
    Department of Pharmacology and Toxicology,Kyorin University School of Medicine,Mitaka,Tokyo 181-8611,Japan
  • Hahn Tae-Won
    Department of Ophthalmology,Catholic University Medical College,Kangnam St.Mary’s Hospital,505 Banpo-dong,Seocho-gu,Seoul 137-701,Korea
  • Sekine Takashi
    Department of Pharmacology and Toxicology,Kyorin University School of Medicine,Mitaka,Tokyo 181-8611,Japan
  • Lee Kweon-Haeng
    Department of Pharmacology,Catholic University Medical College,505 Banpo-dong,Seoul 137-701,Korea
  • Endou Hitoshi
    Department of Pharmacology and Toxicology,Kyorin University School of Medicine,Mitaka,Tokyo 181-8611,Japan

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In the present study, we investigated the effect of adenosine triphosphate(ATP)on cytosolic free calcium mobilization and mitogenic activity in cultured bovine corneal endothelial cells(BCEC).The[Ca2+]i was determined using a Ca2+ sensitive indicator, Fura-2/AM, and cell proliferation was evaluated by counting the cell number.ATP, its metabolites and analogs caused transient increase in[Ca2+]i in a concentration-dependent manner(10-7M−10-3M)and the potency of agonists was ordered as follows:2-methylthio-ATP>uridine triphosphate>ATP>adenosine diphosphate.Adenosine monophosphate and adenosine did not affect[Ca2+]i.ATP(10-4M)also promoted the accumulation of inositol trisphosphate(IP3).The ATP-induced transient[Ca2+]i increase and IP3 accumulation were attenuated by pretreatment with a phospholipase C inhibitor, U-73122(5μM), for 30 min.ATP(10-5M)significantly enhanced the proliferation of BCEC.ATP-induced[Ca2+]i increase and cell proliferation were inhibited by a purinoceptor antagonist, suramin(10-4M).Thus, the present study indicates that BCEC contain P2 purinoceptors that regulate their proliferation.

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