Ogata Y, Niisato N, Negishi T, Sakurai T, Furuyama S, Sugiya H
Department of Periodontology, Nihon University School of Dentistry at Matsudo, Chiba, Japan.
Cell Biol Int. 1995 Aug;19(8):637-45. doi: 10.1006/cbir.1995.1113.
In fura-2-loaded human periodontal ligament (HPDL) cells, bradykinin induced a rapidly transient increase and subsequently sustained increase in cytosolic Ca2+ ([Ca2+]i). When external Ca2+ was chelated by EGTA, the transient peak of [Ca2+]i was reduced and the sustained level was abolished, implying the Ca2+ mobilization consists of intracellular Ca2+ release and Ca2+ influx. Thapsigargin, a specific Ca(2+)-ATPase inhibitor for inositol 1,4,5-trisphosphate (1,4,5-IP3)-sensitive Ca2+ pool, induced an increased in [Ca2+]i in the absence of external Ca2+. After depletion of the intracellular Ca2+ pool by thapsigargin, the increase in [Ca2+]i induced by bradykinin was obviously reduced. Bradykinin also stimulated formation of inositol polyphosphates including 1,4,5-IP3. These results suggest that bradykinin stimulates intracellular Ca2+ release from the 1,4,5-IP3-sensitive Ca2+ pool. Bradykinin stimulated prostaglandin E2 (PGE2) release in the presence of external Ca2+, but not in the absence of external Ca2+. Ca2+ ionophore A23187 and thapsigargin evoked the release of PGE2 in the presence of external Ca2+ despite no activation of bradykinin receptors. These results indicate that bradykinin induces Ca2+ mobilization via activation of phospholipase C and PGE2 release caused by the Ca2+ influx in HPDL cells.
在装载了fura-2的人牙周膜（HPDL）细胞中，缓激肽可诱导细胞溶质Ca2+（[Ca2+]i）迅速短暂升高，随后持续升高。当用乙二醇双四乙酸（EGTA）螯合细胞外Ca2+时，[Ca2+]i的短暂峰值降低，持续水平消失，这意味着Ca2+动员包括细胞内Ca2+释放和Ca2+内流。毒胡萝卜素是一种针对肌醇1,4,5-三磷酸（1,4,5-IP3）敏感Ca2+池的特异性Ca(2+)-ATP酶抑制剂，在无细胞外Ca2+的情况下可诱导[Ca2+]i升高。在用毒胡萝卜素耗尽细胞内Ca2+池后，缓激肽诱导的[Ca2+]i升高明显降低。缓激肽还刺激包括1,4,5-IP3在内的肌醇多磷酸的形成。这些结果表明，缓激肽刺激细胞内Ca2+从1,4,5-IP3敏感Ca2+池中释放。缓激肽在有细胞外Ca2+存在时可刺激前列腺素E2（PGE2）释放，但在无细胞外Ca2+时则不能。尽管未激活缓激肽受体，但Ca2+离子载体A23187和毒胡萝卜素在有细胞外Ca2+存在时可诱发PGE2释放。这些结果表明，缓激肽通过激活磷脂酶C诱导Ca2+动员，并通过HPDL细胞中的Ca2+内流引起PGE2释放。
