HSY-EAl細胞におけるprotease-activated receptor (PAR)-1とPAR-2の相互脱感作機構  [in Japanese] Cross-desensitization between PAR-1 and PAR-2 in HSY-EA 1 cells.  [in Japanese]

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Author(s)

    • 設楽 彰子 SHITARA Akiko
    • 北海道医療大学歯学部歯科薬理学教室 Department of Dental Pharmacology, School of Dentistry, Health Sciences University of Hokkaido
    • 谷村 明彦 TANIMURA Akihiko
    • 北海道医療大学歯学部歯科薬理学教室 Department of Dental Pharmacology, School of Dentistry, Health Sciences University of Hokkaido
    • 根津 顕弘 NEZU Akihiro
    • 北海道医療大学歯学部歯科薬理学教室 Department of Dental Pharmacology, School of Dentistry, Health Sciences University of Hokkaido
    • 森田 貴雄 MORITA Takao
    • 北海道医療大学歯学部歯科薬理学教室 Department of Dental Pharmacology, School of Dentistry, Health Sciences University of Hokkaido
    • 東城 庸介 TOJYO Yosuke
    • 北海道医療大学歯学部歯科薬理学教室 Department of Dental Pharmacology, School of Dentistry, Health Sciences University of Hokkaido

Abstract

The mechanisms for cross-desensitization between protease-activated receptor (PAR)-1 and PAR-2 in human parotid cell line, HSY-EA1 cells were examined. The HSY-EA1 cells strongly expressed mRNAs for PAR-1 and PAR-2, whereas the expression of PAR-3 and PAR-4 was very limited. Stimulation of HSY-EA1 cells with various concentrations of thrombin or trypsin produced a striking increase in [Ca^<2+>]_i followed by a slow return to the basal level within 2-3 min. When cells were pretreated with various concentrations of trypsin, the subsequent Ca^<2+> response with thrombin diminished in a dose-dependent manner over the trypsin concentration, indicating that trypsin desensitized PAR-1. The desensitization of the thrombin-induced Ca^<2+> response was also induced by the pretreatment with PAR-2 agonist peptide, SLIGKV. These results suggest that trypsin-induced inactivation of PAR-1 is due to the heterologous desensitization of PAR-1 through the activation of PAR-2 in addition to a proteolytic degradation of PAR-1.

Journal

  • Higashi Nippon dental journal

    Higashi Nippon dental journal 23(1), 61-67, 2004-06

    Health Sciences University of Hokkaido

Codes

  • NII Article ID (NAID)
    110004689189
  • NII NACSIS-CAT ID (NCID)
    AN0008135X
  • Text Lang
    JPN
  • ISSN
    09109722
  • Data Source
    NII-ELS 
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