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Macrophage migration inhibitory factor limits activation-induced apoptosis of platelets via CXCR7-dependent Akt

Madhumita Chatterjee1, Oliver Borst1, Britta Walker1

  • 1From the Medizinische Klinik III, Kardiologie und Kreislauferkrankungen (M.C., O.B., A.F., S.V., P.S., D.R., T.G., H.F.L., M.G.), Institute of Anatomy (A.M.), and Institute of Physiology (B.W., F.L.), Universität Tübingen, Tübingen, Germany; and Institute of Biochemistry and Molecular Cell Biology, RWTH Aachen University, Uniklinik RWTH Aachen, Aachen, Germany (S.A.-R., J.B.).

Circulation Research
|October 1, 2014
PubMed
Abstract

Insights

Macrophage migration inhibitory factor (MIF) binds to platelet receptor CXCR7, promoting platelet survival and reducing thrombosis. This discovery reveals a new role for MIF in regulating blood clotting and inflammation.

Area of Science:

  • Immunology
  • Hematology
  • Molecular Biology

Background:

  • Macrophage migration inhibitory factor (MIF) is released during platelet activation.
  • The specific role of MIF in platelet function, survival, and thrombotic potential was previously unknown.

Purpose of the Study:

  • To investigate the effects of MIF on platelet survival and thrombotic potential.
  • To identify the receptor and signaling pathways involved in MIF-mediated platelet regulation.

Main Methods:

  • Investigated MIF interaction with platelet receptors CXCR4 and CXCR7.
  • Assessed MIF's impact on platelet apoptosis and activation using in vitro and in vivo models.
  • Utilized knockout (Cxcr7(-/-), Akt(-/-)) and transfected cell lines to elucidate signaling pathways (PI3K-Akt, BAD phosphorylation).
  • Evaluated MIF's effect on thrombus formation under arterial flow and in vivo arterial injury models.

Main Results:

  • Macrophage migration inhibitory factor (MIF) binds to platelet receptor CXCR7, identifying it as a novel MIF receptor on platelets.
  • MIF promotes platelet survival by activating the PI3K-Akt pathway, leading to BAD phosphorylation, independent of CD74.
  • MIF reduces platelet aggregation and thrombus formation in vitro and in vivo, an effect mediated through CXCR7.

Conclusions:

  • MIF binding to CXCR7 modulates platelet survival and thrombotic potential.
  • This interaction suggests MIF plays a significant role in regulating thrombosis and inflammation through platelet pathways.
Keywords:
AktBADMIFapoptosischemokine

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