ArticleThe American journal of pathology2004
CD59a deficiency exacerbates ischemia-reperfusion injury in mice.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 40 citations in OpenAlex.
- The complement system in pediatric acute kidney injury.Pediatric nephrology (Berlin, Germany) · 2023Review
- A potent truncated form of human soluble CR1 is protective in a mouse model of renal ischemia-reperfusion injury.Scientific reports · 2021Article
- Targeted Complement Inhibition Protects Vascularized Composite Allografts From Acute Graft Injury and Prolongs Graft Survival When Combined With Subtherapeutic Cyclosporine A Therapy.Transplantation · 2017Article
- Epidermal growth factor attenuates tubular necrosis following mercuric chloride damage by regeneration of indigenous, not bone marrow-derived cells.Journal of cellular and molecular medicine · 2015Article
- C3a and C5a promote renal ischemia-reperfusion injury.Journal of the American Society of Nephrology : JASN · 2012Article
- Crystal structure of C5b-6 suggests structural basis for priming assembly of the membrane attack complex.The Journal of biological chemistry · 2012Article
- The role of complement in the early immune response to transplantation.Nature reviews. Immunology · 2012Review
- Membrane attack complex inhibitor CD59a protects against focal cerebral ischemia in mice.Journal of neuroinflammation · 2010Article
- Absence of the complement regulatory molecule CD59a leads to exacerbated neuropathology after traumatic brain injury in mice.Journal of neuroinflammation · 2009Article
- Gene silencing of complement C5a receptor using siRNA for preventing ischemia/reperfusion injury.The American journal of pathology · 2008Article
- The mouse complement regulator CD59b is significantly expressed only in testis and plays roles in sperm acrosome activation and motility.Molecular immunology · 2008Article
- The cellular origin and proliferative status of regenerating renal parenchyma after mercuric chloride damage and erythropoietin treatment.Cell proliferation · 2007Article
- Altered renal tubular expression of the complement inhibitor Crry permits complement activation after ischemia/reperfusion.The Journal of clinical investigation · 2006Article
- Targeted complement inhibition by C3d recognition ameliorates tissue injury without apparent increase in susceptibility to infection.The Journal of clinical investigation · 2005Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The terminal complement components C5a and the membrane attack complex are involved in the pathogenesis of ischemia-reperfusion injury in many organs. CD59 is the major regulator of membrane attack complex formation. Mice deficient in the Cd59a gene (mCd59a-/-) were used to investigate the role of CD59 in renal ischemia-reperfusion injury. Unilateral ischemia-reperfusion injury was induced by clamping the left renal pedicle for 30 minutes under general anesthetic. Mice were studied at 72 hours and 2 weeks after ischemia-reperfusion injury. mCd59a-/- mice developed significantly greater tubular injury (P = 0.01), tubulointerstitial apoptosis (P = 0.02), and neutrophil influx (P = 0.04) than controls at 72 hours after ischemia-reperfusion. Two weeks after ischemia-reperfusion, mCd59a-/- mice exhibited more severe tubular damage predominantly in a corticomedullary distribution than controls (P = 0.02). Quantification of interstitial leukocytes revealed significantly greater numbers of infiltrating lymphocytes (but not macrophages) in mCd59a-/- mice than controls (P = 0.04) at 2 weeks. At both time points, significantly more C9 (as a marker of membrane attack complex) deposition occurred in a peritubular distribution in mCd59a-/- mice than controls. In conclusion, these results demonstrate that the lack of CD59a, by allowing unregulated membrane attack complex deposition, exacerbates both the tubular injury and the interstitial leukocyte infiltrate after ischemia-reperfusion injury in mice.
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