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Plasmin triggers chemotaxis of monocyte-derived dendritic cells through an Akt2-dependent pathway and promotes a

Xuehua Li1, Tatiana Syrovets, Felicitas Genze

  • 1Ulm University, Institute of Pharmacology of Natural Products & Clinical Pharmacology, Helmholtzstr. 20, D-89081 Ulm, Germany.

Arteriosclerosis, Thrombosis, and Vascular Biology
|January 9, 2010
PubMed

Insights

Plasmin, an enzyme found in atherosclerotic lesions, prompts dendritic cells (DC) to migrate and activate T cells, potentially worsening atherosclerosis. This study reveals plasmin

Area of Science:

  • Immunology
  • Vascular Biology
  • Cell Biology

Background:

  • Dendritic cells (DC) are present in atherosclerotic arteries and influence the development of atherosclerosis.
  • The role of plasmin in modulating dendritic cell function within the context of atherosclerosis is not well understood.

Purpose of the Study:

  • To investigate the functional effects of plasmin on human dendritic cells (DC).
  • To determine the signaling pathways involved in plasmin-mediated DC activation and migration.
  • To assess the impact of plasmin-stimulated DC on T cell polarization.

Main Methods:

  • Monocyte-derived dendritic cells (DC) were stimulated with plasmin.
  • Actin polymerization, chemotaxis, and intracellular signaling pathways (Akt, MAPK) were analyzed.
  • Short-hairpin RNA (shRNA) was used to knock down Akt1 and Akt2 expression.
  • T cell polarization assays were performed with plasmin-stimulated DC.
  • Immunohistochemistry was used to detect DC and plasmin in human atherosclerotic lesions.

Main Results:

  • Plasmin induced actin polymerization and chemotaxis in DC, similar to formyl-methionyl-leucyl-phenylalanine (fMLP).
  • Plasmin activated Akt and mitogen-activated protein kinases (MAPKs), including p38 and extracellular signal-regulated kinase 1/2 (ERK1/2).
  • Plasmin-induced DC migration required Akt and MAPK activation, specifically Akt2 activation via a p38-dependent pathway.
  • Plasmin-stimulated DC promoted the polarization of CD4(+) T cells towards a pro-inflammatory Th1 phenotype.
  • DC and abundant plasmin were found in human atherosclerotic lesions, often co-localizing.

Conclusions:

  • Plasmin directly influences dendritic cell function, promoting migration and T cell activation.
  • The findings suggest that plasmin generation in atherosclerotic vessels contributes to DC accumulation.
  • Plasmin-mediated DC activation may exacerbate atherosclerosis by promoting an adaptive immune response.
Abstract

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