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MerTK cleavage limits proresolving mediator biosynthesis and exacerbates tissue inflammation.

Bishuang Cai1, Edward B Thorp2, Amanda C Doran1

  • 1Department of Medicine, Columbia University, New York, NY 10032; Department of Pathology and Cell Biology, Columbia University, New York, NY 10032; Department of Physiology, Columbia University, New York, NY 10032;

Proceedings of the National Academy of Sciences of the United States of America
|May 21, 2016
PubMed
Summary

Mer proto-oncogene tyrosine kinase (MerTK) signaling promotes specialized proresolving mediator (SPM) biosynthesis, aiding inflammation resolution. MerTK cleavage limits this process, suggesting therapeutic targets for chronic inflammatory diseases.

Keywords:
5-lipoxygenaseMerTKefferocytosisinflammation resolutionmacrophages

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Area of Science:

  • Immunology
  • Molecular Biology
  • Biochemistry

Background:

  • Inflammation resolution is crucial for tissue homeostasis and preventing chronic disease.
  • Specialized proresolving mediators (SPMs) derived from fatty acids are key to resolution.
  • Regulation of SPM biosynthesis during inflammation and its failure in disease are poorly understood.

Purpose of the Study:

  • To investigate the role of Mer proto-oncogene tyrosine kinase (MerTK) in regulating SPM biosynthesis.
  • To determine how MerTK signaling impacts inflammation resolution in vivo.
  • To explore the functional significance of MerTK cleavage in inflammatory conditions.

Main Methods:

  • Utilized cultured macrophages and mouse models of sterile inflammation and ischemia-reperfusion (I/R) injury.
  • Investigated MerTK signaling pathways affecting 5-lipoxygenase localization.
  • Employed a novel cleavage-resistant MerTK (Mertk(CR)) mouse model.

Main Results:

  • MerTK signaling increases SPM biosynthesis by altering 5-lipoxygenase intracellular localization.
  • MerTK activation promotes resolution of sterile peritonitis and reduces remote organ inflammation after I/R injury.
  • Cleavage-resistant MerTK (Mertk(CR)) enhances SPM levels and improves resolution, reducing lung injury post-I/R.

Conclusions:

  • MerTK-mediated signaling is a critical regulator of SPM biosynthesis and inflammation resolution.
  • Cleavage of MerTK during inflammation limits SPM production and impairs the resolution response.
  • Targeting MerTK cleavage may offer novel therapeutic strategies to enhance resolution in inflammatory diseases.