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Updated: Jun 13, 2025

Multiphoton Intravital Imaging for Monitoring Leukocyte Recruitment during Arteriogenesis in a Murine Hindlimb Model
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Multiphoton Intravital Imaging for Monitoring Leukocyte Recruitment during Arteriogenesis in a Murine Hindlimb Model

Published on: September 30, 2021

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The Complement System Is Essential for Arteriogenesis by Enhancing Sterile Inflammation as a Relevant Step in

Amanda Zhu1,2, Carolin Baur1,2, Philipp Götz1,2

  • 1Institute of Surgical Research at the Walter Brendel Centre of Experimental Medicine, University Hospital, Ludwig-Maximilians-Universität München, 81377 Munich, Germany.

Cells
|September 14, 2024
PubMed

Insights

Complement component C3 is crucial for arteriogenesis, the growth of collateral arteries. Its deficiency impairs blood flow recovery by reducing inflammatory M1-like macrophages and monocyte chemoattractant protein-1 (MCP-1) expression.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Inflammation Research

Background:

  • Arteriogenesis is an inflammatory process involving collateral artery growth to bypass occluded arteries.
  • The complement system component C3 is a known inflammatory activator.

Purpose of the Study:

  • To investigate the role of complement C3 in arteriogenesis using a murine hindlimb model.
  • To determine the impact of C3 deficiency on collateral artery growth and associated inflammatory responses.

Main Methods:

  • Utilized C3-deficient (C3 -/-) and wildtype mice in a femoral artery ligation model.
  • Assessed perfusion recovery using Laser Doppler imaging.
  • Analyzed vascular cell proliferation, macrophage recruitment and polarization (CD68+, M1-like), and gene expression (MCP-1) via immunofluorescence and RT-qPCR.

Main Results:

  • C3 -/- mice exhibited significantly reduced perfusion recovery and vascular cell proliferation.
  • Monocyte chemoattractant protein-1 (MCP-1) expression was significantly lower in C3 -/- mice.
  • While total macrophage recruitment was unaffected, C3 deficiency led to a reduction in M1-like polarized macrophages.
  • Administration of Compound 48/80 or MCP-1 rescued M1-like macrophage numbers and improved perfusion in C3 -/- mice.

Conclusions:

  • Complement C3 plays a critical role in arteriogenesis by promoting MCP-1 expression.
  • MCP-1 is essential for inducing and enhancing sterile inflammation required for effective collateral artery growth.
  • Targeting the C3-mediated inflammatory pathway could be a therapeutic strategy for improving blood flow in ischemic conditions.

Keywords:
arteriogenesiscomplement C3macrophage polarizationmacrophagesmast cellsmonocyte chemoattractant protein-1sterile inflammation

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