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Complement activation and atherosclerosis.

F Niculescu1, H Rus

  • 1Department of Pathology, University of Maryland, School of Medicine, Baltimore 21201, USA. fnicules@umaryland.edu

Molecular Immunology
|March 4, 2000
PubMed
Summary
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The complement system, a key part of inflammation, drives atherosclerosis by recruiting monocytes and activating smooth muscle and endothelial cells. Complement activation significantly contributes to atherosclerotic lesion development and progression.

Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Cell Biology

Background:

  • Atherosclerosis is an inflammatory disease involving monocytes/macrophages, complement, and T-lymphocytes.
  • Complement activation in the arterial wall releases factors that recruit monocytes and can cause cell lysis or activation.
  • Sublytic assembly of the membrane attack complex (C5b-9) on arterial cells promotes activation and proliferation.

Purpose of the Study:

  • To investigate the role of complement activation in atherosclerosis.
  • To analyze the signaling pathways activated by C5b-9 in arterial cells.

Main Methods:

  • Analysis of mitogen-activated protein kinase (MAPK) pathways in smooth muscle cells (SMC) exposed to C5b-9.
  • Investigating Janus kinase (JAK) and signal transducer and activator of transcription (STAT) activation in endothelial cells (EC) upon C5b-9 assembly.

Related Experiment Videos

  • Utilizing wortmannin to assess the involvement of phosphatidylinositol-3 (PI 3-) kinase in ERK1 activation.

    • Main Results:

    • C5b-9 activated extracellular signal-regulated kinase (ERK) 1, c-jun NH2-terminal kinase (JNK) 1, and p38 MAPK in aortic SMC.
    • ERK1 activation was dependent on PI 3-kinase.
    • Sublytic C5b-9 assembly activated JAK1, STAT3, and STAT4 in EC, with JAK1 activation being Gi protein-dependent.

    Conclusions:

    • Complement activation plays a crucial role in both the initiation and progression of atherosclerotic lesions.
    • The complement system is a central component of the chronic inflammation observed in atherosclerosis.
    • C5b-9 signaling pathways in SMC and EC contribute to the inflammatory processes underlying atherosclerosis.