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signal transduction of epithelial cells in response to secretagogues

Research Project

Project/Area Number 15591806
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Otorhinolaryngology
Research InstitutionMie University

Principal Investigator

KISHIOKA Chikako  Mie University, Faculty of Medicine, Research Associate, 医学部, 助手 (10314113)

Co-Investigator(Kenkyū-buntansha) TAKEUCHI Kazuhiko  Mie University, Faculty of Medicine, Associate Professor, 医学部, 助教授 (50206942)
Project Period (FY) 2003 – 2004
Project Status Completed (Fiscal Year 2004)
Budget Amount *help
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 2004: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
Keywordsmucin / secretion / signal transduction / ムキン
Research Abstract

Chronic obstructive airway disease is marked by excess production of airway mucus. The molecular mechanisms underlying this pathology are unknown. ATP and PAF are detected in inflamed airways, and suggested to contribute to mucus overproduction. We examined the possibility that ATP and PAF contributes to mucus hypersecretion. Result in cultured cells showed that MUC5AC expression increased in response to ATP and PAF. These appeared to be mediated by intracellular pathways involving JNK/PKA/CREB for ATP and MAPK/JNK for PAF. (We used reporter assay and specific inhibitors.) Such identification of pathways involved in MUC5AC up-regulation by ATP and PAF in the HM3 cells may serve as a model for the effects of cytokines and mediators, which regulate MUC5AC expression during the airway inflammation.

Report

(3 results)
  • 2004 Annual Research Report   Final Research Report Summary
  • 2003 Annual Research Report

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Published: 2003-04-01   Modified: 2016-04-21  

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