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Soluble P-selectin moderates complement dependent injury.

S A Woodcock1, C Kyriakides, Y Wang

  • 1Department of Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.

Shock (Augusta, Ga.)
|December 29, 2000
PubMed
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Soluble P-selectin (sPsel) moderates complement activation by inhibiting the classical pathway. This finding is crucial for understanding and treating reperfusion injury in models involving intestinal and hindlimb ischemia.

Area of Science:

  • Immunology
  • Physiology

Background:

  • P-selectin, an adhesion molecule on activated platelets and endothelium, possesses short consensus repeats (SCRs) similar to complement regulatory proteins.
  • Ischemia-reperfusion injury, particularly in the intestine, is often mediated by the classical complement pathway.

Purpose of the Study:

  • To investigate the role of P-selectin's SCRs in moderating complement responses during ischemia-reperfusion injury.
  • To confirm the hypothesis using murine models of both intestinal and hindlimb ischemia-reperfusion.

Main Methods:

  • Comparison of intestinal and hindlimb permeability in P-selectin deficient (P-/-) mice versus wild-type (P+/+) mice.
  • Assessment of injury following reconstitution of P-/- mice with either P+/+ or P-/- platelets.
  • Measurement of complement component 50 (CH50) levels after intestinal ischemia-reperfusion to evaluate complement activation and consumption.

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Main Results:

  • Mice deficient in P-selectin showed similar permeability to wild-type mice in both intestinal and hindlimb ischemia-reperfusion models.
  • Reconstitution with P+/+ platelets, but not P-/- platelets, significantly reduced permeability in P-/- mice subjected to intestinal (29%) and hindlimb (33%) ischemia-reperfusion.
  • Intestinal ischemia-reperfusion led to a significant fall in CH50 in P-/- mice, indicating complement activation, which was blunted in animals reconstituted with P+/+ platelets.

Conclusions:

  • Soluble P-selectin (sPsel) moderates complement activation by competing with C1q binding to antibodies.
  • This interaction limits the activation of the classical complement pathway, which mediates murine reperfusion injury.
  • sPsel represents a potential therapeutic target for mitigating ischemia-reperfusion damage.