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首页> 外文期刊>Cell biology international. >EFFECTS OF BRADYKININ ON CA2+ MOBILIZATION AND PROSTAGLANDIN E(2) RELEASE IN HUMAN PERIODONTAL LIGAMENT CELLS
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EFFECTS OF BRADYKININ ON CA2+ MOBILIZATION AND PROSTAGLANDIN E(2) RELEASE IN HUMAN PERIODONTAL LIGAMENT CELLS

机译:缓激肽对人牙周膜细胞中CA2 +移动和前列腺素E(2)释放的影响

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摘要

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 Ca2+-ATPase inhibitor for inositol 1,4,5-trisphosphate (1,4,5-IP3)-sensitive Ca2+ pool, induced an increase 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 E(2) (PGE(2)) release in the presence of external Ca2+, but not in the absence of external Ca2+. Ca2+ ionophore A23187 and thapsigargin evoked the release of PGE(2) 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 PGE(2) release caused by the Ca2+ influx in HPDL cells.
机译:在呋喃2加载的人牙周膜(HPDL)细胞中,缓激肽诱导细胞内Ca2 +([Ca2 +](i))的快速瞬时增加并随后持续增加。当外部Ca2 +被EGTA螯合时,[Ca2 +](i)的瞬时峰减少,维持水平被消除,这意味着Ca2 +的动员包括细胞内Ca2 +的释放和Ca2 +的涌入。 Thapsigargin是肌醇1,4,5-三磷酸(1,4,5-IP3)敏感的Ca2 +库的一种特定的Ca2 + -ATPase抑制剂,可在没有外部Ca2 +的情况下诱导[Ca2 +](i)的增加。 thapsigargin耗尽了细胞内Ca2 +库后,缓激肽诱导的[Ca2 +](i)的增加明显减少。缓激肽还刺激肌醇多磷酸盐包括1,4,5-IP3的形成。这些结果表明缓激肽刺激细胞内Ca2 +从1,4,5-IP3敏感的Ca2 +库中释放。缓激肽在存在外部Ca2 +的情况下刺激前列腺素E(2)(PGE(2))释放,但是在没有外部Ca2 +的情况下则不会。尽管没有缓激肽受体的激活,Ca2 +离子载体A23187和thapsigargin引起了外部Ca2 +存在下PGE(2)的释放。这些结果表明缓激肽通过激活磷脂酶C和由HPDL细胞中Ca2 +流入引起的PGE(2)释放来诱导Ca2 +动员。

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