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RAGE : Its pahotphysiological role in the lung injury and a biomarker of acute lung injury

Research Project

Project/Area Number 17591618
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Anesthesiology/Resuscitation studies
Research InstitutionTokyo Medical and Dental University

Principal Investigator

UCHIDA Tokujiro  Tokyo Medical and Dental Univ., Assistant Professor, 医学部附属病院, 講師 (40262183)

Project Period (FY) 2005 – 2006
Project Status Completed (Fiscal Year 2006)
Budget Amount *help
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2005: ¥2,800,000 (Direct Cost: ¥2,800,000)
Keywordslung injury / biomarker / pulmonary edema / 急性呼吸窮迫症候群 / 肺胞上皮 / RAGE / 重症度マーカー
Research Abstract

Rationale : Receptor for advanced glycation end-products (RAGE) is one of the alveolar type I cell associated proteins in the lung.
Objectives : To test the hypothesis that RAGE is a marker of alveolar epithelial type I cell injury.
Methods : Rats were instilled intratracheally with either 10 mg/kg lipopolysaccharide (LPS) or hydrochloric acid. RAGE levels were measured in the bronchoalveolar lavage (BAL) and serum in the rats and in the pulmonary edema fluid and plasma from patients with acute lung injury (ALI) (n=22) and hydrostatic pulmonary edema (n=11).
Main Results : In the rat lung injury studies, RAGE was released into the BAL and serum as a single soluble isoform sized 〜48 kD. The elevated levels of RAGE in the BAL correlated well with the severity of experimentally induced lung injury. In the human studies, the RAGE level in the pulmonary edema fluid was significantly higher than the plasma level (p<0.0001). The median edema fluid / plasma ratio of RAGE levels was 105 (IQR;55-243). The RAGE levels in the pulmonary edema fluid from patients with ALI were higher than the levels from patients with hydrostatic pulmonary edema (p<0.05), and the plasma RAGE level in patients with ALI were significantly higher than the healthy volunteers (p<0.001) or patients with hydrostatic pulmonary edema (p<0.05).
Conclusion : RAGE is a marker of type I alveolar epithelial cell injury based on experimental studies in rats as well as in patients with acute lung injury.

Report

(3 results)
  • 2006 Annual Research Report   Final Research Report Summary
  • 2005 Annual Research Report
  • Research Products

    (3 results)

All 2006

All Journal Article (3 results)

  • [Journal Article] Receptor for advanced glycation end-products is a marker of type I cell injury in acute lung injury.2006

    • Author(s)
      Uchida T, Shirasawa M, Ware LB et al.
    • Journal Title

      Am J Respir Crit Care Med. 173

      Pages: 1008-1015

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Receptor for advanced glycation end-products is a marker of type I cell injury in acute lung injury.2006

    • Author(s)
      Uchida T, Shirasawa M, Ware LB et al.
    • Journal Title

      Vol 173.

      Pages: 1008-1015

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Receptor for advanced glycation end-products is a marker of type I cell injury in actue lung injury.2006

    • Author(s)
      Uchida T, Shirasawa M, Ware LB, et al.
    • Journal Title

      Am J Respir Crit Care Med. 173

      Pages: 1008-1015

    • Related Report
      2006 Annual Research Report

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Published: 2005-04-01   Modified: 2016-04-21  

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