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Histamine H 1 receptor‐stimulated Ca 2+ signaling pathway in human periodontal ligament cells
Author(s) -
Niisato N.,
Ogata Y.,
Furuyama S.,
Sugiya H.
Publication year - 1996
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1996.tb00472.x
Subject(s) - histamine , thapsigargin , extracellular , chemistry , endocrinology , medicine , cimetidine , histamine h2 receptor , intracellular , histamine receptor , inositol , histaminergic , histamine h1 receptor , antagonist , receptor , biochemistry , biology
We studied histamine‐induced Ca 2+ mobilization in human periodontal ligament (HPDL) cells. Histamine induced a transient rise in intracellular Ca 2+ ([Ca 2+ ] i ) and maintained a sustained phase in the presence of extracellular Ca 2+ . In the absence of extracellular Ca 2+ , the transient peak was slightly reduced and the sustained phase was decreased to the basal level. The initial rise in [Ca 2+ ] i was attributed to two components: intracellular Ca 2+ release and Ca 2+ influx, whereas the sustained phase was due to Ca 2+ influx. After depletion of intracellular Ca 2+ stores with thapsigargin, a known Ca 2+ ‐ATPase inhibitor, histamine‐induced increase in [Ca 2+ ] i was significantly reduced, suggesting histamine induces Ca 2+ release from inositol 1,4,5‐trisphosphate [Ins(l,4,5)P 3 ]‐ and thapsigargin‐sensitive Ca 2+ stores. Histamine‐induced peak in [Ca 2+ ] i was increased dose‐dependently in the presence and absence of extracellular Ca 2+ . The histamine‐mediated response in [Ca 2+ ] i was specifically attenuated by chlorpheniramine (H 1 antagonist) but not by cimetidine (H 2 antagonist), clearly indicating that activation of H 1 receptor mediates histamine‐induced Ca 2+ mobilization. We next examined the effect of histamine on inositol phosphates formation. Histamine stimulated the formation of inositol phosphates which changed time‐dependently. In particular, the formation of Ins(1,4,5)P 3 was increased significantly for 10 s. The histamine‐induced Ca 2+ mobilization caused an increase of prostaglandin E 2 (PGE 2 ) release which was reduced in excluding extracellular Ca 2+ . These results indicate that activation of histamine H 1 receptor induces the accumulation of Ins(l,4,5)P 3 and the following transient increase in [Ca 2+ ] i , and elicits the release of PGE 2 which may be coupled with Ca 2+ influx.