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The extracellular matrix protein mindin serves as an integrin ligand and is critical for inflammatory cell

Wei Jia1, Hong Li, You-Wen He

  • 1Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA.

Blood
|August 18, 2005
PubMed

Insights

Mice lacking the extracellular matrix (ECM) protein mindin show reduced inflammatory cell recruitment. Mindin acts as a novel ligand for integrins, crucial for inflammatory cell migration during inflammation.

Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Leukocyte recruitment to inflammation sites is essential for immune response.
  • Integrin-extracellular matrix (ECM) interactions mediate leukocyte adhesion and migration.
  • The specific role of ECM proteins like mindin in leukocyte recruitment remains largely undefined.

Purpose of the Study:

  • To investigate the role of the ECM protein mindin in inflammatory cell recruitment.
  • To identify the molecular interactions between mindin and inflammatory cells.
  • To determine the functional significance of mindin-integrin interactions in vivo.

Main Methods:

  • Generation and analysis of mice lacking the mindin gene.
  • Assessment of neutrophil and macrophage recruitment in multiple inflammation models.
  • In vitro assays for neutrophil adhesion to immobilized mindin.
  • Migration assays using mindin matrix.
  • Flow cytometry and cell adhesion assays using transfected HEK-293 cells and anti-integrin antibodies.

Main Results:

  • Mice lacking mindin exhibited severely impaired recruitment of neutrophils and macrophages in four different inflammation models.
  • Neutrophils directly bind to immobilized mindin, and mindin matrix mediates neutrophil migration in vitro.
  • Neutrophil adhesion to mindin was blocked by antibodies against integrin alpha4, alphaM, and beta2.
  • HEK-293 cells expressing these integrins showed enhanced binding to mindin, which was blocked by anti-integrin antibodies.

Conclusions:

  • Mindin serves as a novel ligand for specific integrins (alpha4, alphaM, beta2).
  • Mindin-integrin interactions are critical for inflammatory cell recruitment in vivo.
  • These findings highlight a new mechanism regulating immune cell trafficking during inflammation.

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