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Evidence of an interaction between TGF-β1 and the SDF-1/CXCR4/CXCR7 axis in human platelets

Dominik Rath1, Madhumita Chatterjee1, Annabell Holtkamp1

  • 1Department of Cardiology, University Hospital Tuebingen, Otfried-Mueller-Straße 10, Tuebingen, Germany.

Thrombosis Research
|June 18, 2016
PubMed

Insights

Platelets express TGF-β1 and SDF-1/CXCR4/CXCR7, which interact in coronary artery disease (CAD). SDF-1 stimulation increases TGF-β1 on platelets, suggesting a novel signaling pathway in CAD.

Area of Science:

  • Cardiovascular Biology
  • Platelet Signaling
  • Molecular Medicine

Background:

  • Transforming growth factor-beta 1 (TGF-β1), stromal cell-derived factor-1 (SDF-1), and its receptors CXCR4 and CXCR7 are present on human platelets.
  • Expression levels of these molecules are altered in symptomatic coronary artery disease (CAD) and influence patient outcomes.
  • The interplay between TGF-β1 and the SDF-1/CXCR4/CXCR7 axis in platelets, particularly in the context of CAD, remains poorly understood.

Purpose of the Study:

  • To investigate the potential crosstalk between TGF-β1 and the SDF-1/CXCR4/CXCR7 axis within human platelets.
  • To provide clinical and experimental evidence for interactions between these signaling molecules in the context of CAD.

Main Methods:

  • Analysis of platelet surface expression of TGF-β1, SDF-1, CXCR4, and CXCR7 in 284 CAD patients using flow cytometry.
  • In vitro stimulation assays using platelet-rich plasma treated with TGF-β1 or SDF-1, followed by flow cytometry analysis.
  • Multiple regression analyses to determine independent associations between TGF-β1 and SDF-1/CXCR4/CXCR7, considering clinical cofactors.

Main Results:

  • CXCR4 and CXCR7 expression significantly predicted TGF-β1 levels (p<0.001 for both).
  • SDF-1 stimulation led to a significant increase in platelet surface TGF-β1 expression (mean MFI 19.01 vs. 14.01, p<0.001).
  • Blocking CXCR4 or CXCR7 receptors with monoclonal antibodies significantly blunted the SDF-1-induced increase in TGF-β1 expression, while TGF-β1 stimulation did not affect SDF-1, CXCR4, or CXCR7 expression.

Conclusions:

  • This study presents the first clinical and experimental evidence of a cross-talk between TGF-β1 and the SDF-1/CXCR4/CXCR7 axis in human platelets.
  • This interaction does not appear to involve transcriptional modulation, differing from findings in other cellular systems.
Abstract

Keywords:
CXCL12CXCR4CXCR7 protein, humanPlateletsTGFbeta1

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