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Interactions between integrin α9β1 and VCAM-1 promote neutrophil hyperactivation and mediate poststroke DVT.

Nilesh Pandey1, Harpreet Kaur1, Mehul R Chorawala2

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Stroke increases the risk of deep vein thrombosis (DVT). Neutrophil integrin α9 and VCAM-1 promote DVT after stroke by enhancing neutrophil adhesion and hyperactivation. Macitentan inhibits this pathway, reducing DVT severity.

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Area of Science:

  • Cardiovascular Biology
  • Hematology
  • Immunology

Background:

  • Venous thromboembolic events, particularly deep vein thrombosis (DVT), are major complications following stroke.
  • Neutrophils play a critical role in the early response to stroke and are implicated in DVT pathogenesis.
  • Integrin α9 on neutrophils mediates adhesion to vascular cell adhesion molecule 1 (VCAM-1) on activated endothelium.

Purpose of the Study:

  • To investigate the role of neutrophil integrin α9 in the development of DVT after stroke.
  • To elucidate the molecular mechanisms by which integrin α9 contributes to poststroke DVT.
  • To identify potential therapeutic targets for preventing or treating poststroke DVT.

Main Methods:

  • Measurement of neutrophil integrin α9 and plasma VCAM-1 levels in human and mouse stroke models.
  • Assessment of DVT severity in neutrophil-specific integrin α9-deficient mice and wild-type littermates following embolic stroke.
  • Transcriptomic analysis to identify pathways regulated by α9/VCAM-1 interactions.
  • Mechanistic studies on neutrophil adhesion, activation, and endothelial cell apoptosis.
  • In vitro screening and validation of macitentan as an inhibitor of α9/VCAM-1 interactions.

Main Results:

  • Elevated neutrophil integrin α9 and plasma VCAM-1 were observed in stroke patients and mice.
  • Neutrophil-specific integrin α9 deficiency significantly reduced DVT severity, neutrophil infiltration, and citrullinated histone H3 in thrombi.
  • α9/VCAM-1 interactions were linked to pathways of neutrophil inflammation, exocytosis, NF-κB signaling, and chemotaxis.
  • Integrin α9/VCAM-1 signaling promoted neutrophil adhesion, hyperactivation, ERK phosphorylation, and endothelial cell apoptosis.
  • Macitentan effectively inhibited α9/VCAM-1 interactions and neutrophil adhesion, reducing DVT severity in control mice but not in α9-deficient mice.

Conclusions:

  • Neutrophil integrin α9 is a critical mediator of DVT development following stroke.
  • The α9/VCAM-1 axis promotes neutrophil hyperactivation and adhesion, contributing to poststroke DVT.
  • Macitentan emerges as a potential therapeutic agent for poststroke DVT by targeting the α9/VCAM-1 pathway.