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Analysis of the role of signaling suppressor SOCS3 in the development of atherosclerosis

Research Project

Project/Area Number 16590723
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Circulatory organs internal medicine
Research InstitutionKurume University

Principal Investigator

YASUKAWA Hideo  Kurume University, Cardiovascular Research institute, Assistant Professor, 循環器病研究所, 講師 (60289361)

Co-Investigator(Kenkyū-buntansha) IMAIZUMI Tsutomu  Kurume University, School of Medicine, Professor, 医学部, 教授 (60148947)
KAI Hisashi  Kurume University, School of Medicine, Associate Professor, 医学部, 助教授 (60281531)
Project Period (FY) 2004 – 2005
Project Status Completed (Fiscal Year 2005)
Budget Amount *help
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥2,200,000 (Direct Cost: ¥2,200,000)
Keywordsatherosclerosis / macrophage / SOCS / STAT3 / Interleukin-6 / サイトカイン / JAK / STAT / SOCS3 / 酸化LDL / マクロファージ泡沫化
Research Abstract

STAT3 was phosphorylated in the aorta from ApoE deficient mice on high fat diet. On the other hand, phosphorylation of STAT3 was not observed in the aorta from control mice. Immunostatining revealed that STAT3 were mainly phosphorylated in macrophages and endothelial cells of plaque from ApoE deficient mice on high fat diet. RT-PCR analysis showed that IL-6, oncostatin M and SOCS3 (suppressor of cytokine signaling) were significantly induced in aorta from Apo deficient mice compared with wild type mice. LIF(leukemia inhibitory factor) and IL-10 were not expressed in control mice and ApoE deficient mice. These results suggest that gp130 cytokines IL-6 and oncostatin M activate JAK-STAT3 pathway that is negatively regulated by SOCS3. To evaluate the role of IL-6 on foam cell formation of macrophages, we examined the effect of IL-6 on oxidized-LDL (oxLDL) uptake by murine peritoneal macrophages in vitro. IL-6 stimulation significantly increased the incorporation of Dil-labeled oxLDL of macrophages. These data suggest that IL-6-STAT3 pathway is activated during the development of atherosclerosis and may contribute to foam cell formation of macrophages.

Report

(3 results)
  • 2005 Annual Research Report   Final Research Report Summary
  • 2004 Annual Research Report
  • Research Products

    (3 results)

All 2004

All Journal Article (3 results)

  • [Journal Article] Small proline-rich protein 1A is a gp130 pathway- and stress-inducible cardioprotective protein2004

    • Author(s)
      Pardervand S, Yasukawa H, (他16名, 2番目)
    • Journal Title

      EMBO J 23(22)

      Pages: 4517-4525

    • Related Report
      2004 Annual Research Report
  • [Journal Article] SOCS3 deficiency in the brain elevates leptin sensitivity and confers resistance to diet-induced obesity2004

    • Author(s)
      Mori H, Yasukawa H, (他9名, 9番目)
    • Journal Title

      Nature Med 10(7)

      Pages: 739-743

    • Related Report
      2004 Annual Research Report
  • [Journal Article] SOCS3 is a physiological negative regulator for granulopoiesis and granulocyte colony-stimulating factor receptor signaling2004

    • Author(s)
      Kimura A, Yasukawa H, (他8名, 8番目)
    • Journal Title

      J Biol Chem 279(8)

      Pages: 6905-6910

    • Related Report
      2004 Annual Research Report

URL: 

Published: 2004-04-01   Modified: 2016-04-21  

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