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THE EFFECTS OF ENDOTHELIN ON ENOTIN-INDUCED PULMONARY VASCULAR IACM-1 EXPRESSION AND ITS APPLICATION TO THE THERAPEUTIC STRATEGY OF ACUTE LUNG INJURY

Research Project

Project/Area Number 10671446
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Anesthesiology/Resuscitation studies
Research InstitutionTeikyo University

Principal Investigator

MORITA Shigeho  TEIKYO UNIVERSITY SCHOOL OF MEDICINE, PROFESSOR, 医学部, 教授 (60143476)

Co-Investigator(Kenkyū-buntansha) GOTO Yukiko  TEIKYO UNIVERSITY SCHOOL OF MEDICINE, STAFF ASSISTANT, 医学部, 助手 (20276710)
TAKADA Shinji  TEIKYO UNIVERSITY SCHOOL OF MEDICINE, STAFF ASSISTANT, 医学部, 助手 (90226788)
市瀬 史  帝京大学, 医学部, 講師 (40276712)
上園 昌一  帝京大学, 医学部, 講師 (10291676)
Project Period (FY) 1998 – 1999
Project Status Completed (Fiscal Year 1999)
Budget Amount *help
¥3,900,000 (Direct Cost: ¥3,900,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥3,400,000 (Direct Cost: ¥3,400,000)
Keywordsadhesion molecule / acute lung injury / endothelin / Nitric Oxide / transcriptional nuclear factor / エンドトキシン
Research Abstract

Endothelin-1 (ET-1) and Nitric Oxide (NO) play an opposing role in the control of pulmonary vascular tone. Recently, these vasoactive substances have recognized as homeostatic regulator of local vascular endothelial cells. At the site of inflammation, vascular endothelial cells are activated and endothelial-leukocyte adhesion molecules such as intercellular adhesion molecule-l (ICAM-1) are up regulated on the surface of endothelial cells.
In this project, we examined the impact of ET-1 and NO on ICAM-1 expression on cultured human pulmonary microvascular endothelial cells (HPMVEC). The results are summarized as below:
1. Under unstimulated state, neither ET-1 nor NO had any effects on ICAM-1 expression on HPMVEC.
2. NO inhibited endotoxin (LPS)-stimulated ICAM-1 expression in a dose dependent manner by 30-50% as determined by cell surface enzyme immunoassays. In contrast, ET-1 had no effect on LPS-stimulated ICAM-1 expression.
3. Immunofluorescence study indicates that the mechanism by which NO inhibits ICAM-1 expression, in part, involves inhibition of transnuclear location transcriptional nuclear factor-CB (NF-κB).
Several lines of evidence have recently suggested a role for NO as an antileukocyte autacoid. Our present study provides a link between NO and leukocyte and offers clues as to the mechanism of such an effect. We speculate development of modulatory strategies targeting NF-κB my provide a novel therapeutic tool for the treatment of lung inflammatory disease.

Report

(3 results)
  • 1999 Annual Research Report   Final Research Report Summary
  • 1998 Annual Research Report

URL: 

Published: 1998-04-01   Modified: 2016-04-21  

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