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Deficiency of plasminogen receptor, Plg-RKT , causes defects in plasminogen binding and inflammatory macrophage

L A Miles1, N Baik1, S Lighvani1

  • 1Department of Cell and Molecular Biology, The Scripps Research Institute, La Jolla, CA, USA.

Journal of Thrombosis and Haemostasis : JTH
|October 8, 2016
PubMed

Insights

Plasminogen Receptor KT (Plg-RKT) is crucial for macrophage recruitment in inflammation. Its absence leads to offspring mortality, indicating a vital role in species survival and lactation.

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Plg-RKT is a novel integral membrane plasminogen receptor.
  • It binds plasminogen and promotes its activation on the cell surface.
  • Its in vivo functions were previously unknown.

Purpose of the Study:

  • To investigate the in vivo role of Plg-RKT.
  • To characterize the effects of Plg-RKT deficiency on reproduction, viability, and inflammatory responses.

Main Methods:

  • Generation of Plg-RKT knockout (Plg-RKT-/-) mice using homologous recombination.
  • Assessment of reproductive success, offspring survival, and inflammatory responses (peritonitis model).

Main Results:

  • Plg-RKT-/- mice were viable and fertile, but all offspring died within 2 days of birth due to maternal lactation defects.
  • Female Plg-RKT-/- mice showed altered growth rates.
  • Plg-RKT deficiency resulted in impaired macrophage recruitment and reduced plasminogen binding capacity.

Conclusions:

  • Plg-RKT is essential for plasminogen binding and macrophage migration in vivo.
  • Plg-RKT deficiency is incompatible with species survival due to reproductive failure.
  • The generated Plg-RKT knockout mouse model is valuable for studying cell surface plasminogen activation in vivo.
Keywords:
cell surfaceinflammationperitonisplasminogenreceptorsthioglycolates

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