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Angiotensin II induces CD62L shedding in human neutrophils

Antonio Vega1, Rajaa El Bekay, Pedro Chacón

  • 1Servicio Regional de Inmunología y Alergia, Hospital Universitario Virgen Macarena, Sevilla, Spain.

Atherosclerosis
|October 20, 2009
PubMed

Insights

Angiotensin II (Ang II) reduces CD62L on neutrophils, a key step in atherosclerosis. This process involves AT1 receptors and specific signaling pathways, independent of neutrophil adhesion.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Molecular Biology

Background:

  • Atherosclerosis pathogenesis involves leukocyte adhesion molecules and the renin-angiotensin system in hypertension.
  • Understanding molecular mechanisms regulating leukocyte-endothelial interactions is crucial.

Purpose of the Study:

  • To investigate the effect of angiotensin II (Ang II) on CD62L expression in human neutrophils.
  • To elucidate the signaling pathways mediating Ang II's regulation of CD62L.

Main Methods:

  • Human neutrophils were stimulated with Ang II.
  • Cell surface CD62L expression was measured using flow cytometry.
  • Involvement of AT1-receptor antagonists and protein kinase inhibitors was assessed.

Main Results:

  • Angiotensin II (Ang II) significantly down-regulated CD62L expression on human neutrophils.
  • This CD62L shedding was independent of neutrophil adhesion to endothelial cells.
  • The process involved AT1 receptors, ERK1/2 MAPK, PI3K, and calcineurin, but not p38 MAPK or small GTPases.

Conclusions:

  • Angiotensin II directly modulates neutrophil CD62L expression via specific intracellular signaling pathways.
  • These findings offer new insights into the role of the renin-angiotensin system in inflammatory processes of atherosclerosis.

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