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Complement component C3 mediates inflammatory injury following focal cerebral ischemia

J Mocco1, William J Mack, Andrew F Ducruet

  • 1Department of Neurosurgery, Columbia University, 710 W 168th St, New York, NY 10032, USA.

Circulation Research
|June 17, 2006
PubMed

Insights

Complement component 3 (C3) activation is critical for stroke-related inflammation and injury. Inhibiting C3 or its receptor reduces infarct volume and neurological deficits in stroke models.

Area of Science:

  • Neuroscience
  • Immunology
  • Cardiovascular Research

Background:

  • Complement cascade activation contributes to ischemia/reperfusion injury, particularly in acute stroke.
  • Understanding specific complement subcomponents involved in post-ischemic injury is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the role of complement proteins C1q, C3, and C5 in focal cerebral ischemia.
  • To determine if C3 activation is a key mediator of stroke-related inflammatory injury.

Main Methods:

  • Transient focal cerebral ischemia was induced in mice deficient in C1q, C3, or C5.
  • Infarct volume, neurological deficit scores, granulocyte infiltration, and oxidative stress were assessed.
  • The effect of a C3a-receptor antagonist was evaluated.

Main Results:

  • Only C3-deficient mice showed significant protection, with 34% reductions in infarct volume and neurological deficits.
  • C3 deficiency led to decreased granulocyte infiltration and reduced oxidative stress.
  • C3a-receptor antagonist administration mirrored these protective effects.

Conclusions:

  • Complement component 3 (C3) activation is the primary driver of complement-mediated inflammatory injury following stroke.
  • Targeting C3 activation or its receptor offers a promising therapeutic strategy for acute stroke.

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