Effects of bradykinin on Ca2+ mobilization and prostaglandin E2 release in human periodontal ligament cells.

✍ Scribed by Yorimasa Ogata; Naomi Niisato; Tetsuo Negishi; Takeshi Sakurai; Shunsuke Furuyama; Hiroshi Sugiya

• Publisher: Elsevier Science
• Year: 1995
• Tongue: English
• Weight: 400 KB
• Volume: 19
• Category: Article
• ISSN: 1065-6995
• DOI: 10.1006/cbir.1995.1113

✦ Synopsis

Abstract

In fura‐2‐loaded human periodontal ligament (HPDL) cells, bradykinin induced a rapidly transient increase and subsequently sustained increase in cytosolic Ca^2+^ ([Ca^2+^]~i~). When external Ca^2+^ was chelated by EGTA, the transient peak of [Ca^2+^]~i~ was reduced and the sustained level was abolished, implying the Ca^2+^ mobilization consists of intracellular Ca^2+^ release and Ca^2+^ influx. Thapsigargin, a specific Ca^2+^‐ATPase inhibitor for inositol 1,4,5‐trisphosphate (1,4,5‐1P~3~)‐sensitive Ca^2+^ pool, induced an increase in [Ca^2+^]~i~ in the absence of external Ca^2+^. After depletion of the intracellular Ca^2+^ pool by thapsigargin, the increase in [Ca^2+^]~i~ induced by bradykinin was obviously reduced. Bradykinin also stimulated formation of inositol polyphosphates including 1,4,5‐IP~3~. These results suggest that bradykinin stimulates intracellular Ca^2+^ release from the 1,4,5‐1P~3~‐sensitive Ca^2+^ pool. Bradykinin stimulated prostaglandin E~2~ (PGE~2~) release in the presence of external Ca^2+^, but not in the absence of external Ca^2+^. Ca^2+^ ionophore A23187 and thapsigargin evoked the release of PGE~2~ in the presence of external Ca^2+^ despite no activation of bradykinin receptors. These results indicate that bradykinin induces Ca^2+^ mobilization via activation of phospholipase C and PGE~2~ release caused by the Ca^2+^ influx in HPDL cells.