ArticleKidney international2014
Tissue-specific deletion of Crry from mouse proximal tubular epithelial cells increases susceptibility to renal ischemia-reperfusion injury.
Article in Kidney international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Rationale for Targeting Complement to Mitigate Renal Transplant Ischemia-Reperfusion Injury.Journal of the American Society of Nephrology : JASN · 2026Review
- Germacrone Ameliorates Diabetic Kidney Disease by Activating TFEB to Promote Autophagy and Inhibit Inflammation.ACS omega · 2025Article
- Friend or foe: assessing the value of animal models for facilitating clinical breakthroughs in complement research.The Journal of clinical investigation · 2025Review
- Dual role of complement in neuronal repair.Frontiers in immunology · 2025Review
- Infiltrating myeloid cell-derived properdin markedly promotes microglia-mediated neuroinflammation after ischemic stroke.Journal of neuroinflammation · 2023Article
- Mild Hypothermia Alleviates Complement C5a-Induced Neuronal Autophagy During Brain Ischemia-Reperfusion Injury After Cardiac Arrest.Cellular and molecular neurobiology · 2023Article
- Role of Complement System in Kidney Transplantation: Stepping From Animal Models to Clinical Application.Frontiers in immunology · 2022Review
- Reduced Neutrophil Extracellular Trap Formation During Ischemia Reperfusion Injury in C3 KO Mice: C3 Requirement for NETs Release.Frontiers in immunology · 2022Article
- Properdin Deficiency Impairs Phagocytosis and Enhances Injury at Kidney Repair Phase Post Ischemia-Reperfusion.Frontiers in immunology · 2021Article
- Complement Initiation Varies by Sex in Intestinal Ischemia Reperfusion Injury.Frontiers in immunology · 2021Article
- Circulating FH Protects Kidneys From Tubular Injury During Systemic Hemolysis.Frontiers in immunology · 2020Article
- The role of properdin in complement-mediated renal diseases: a new player in complement-inhibiting therapy?Pediatric nephrology (Berlin, Germany) · 2019Article
- Complement Inhibitor CRIg/FH Ameliorates Renal Ischemia Reperfusion Injury via Activation of PI3K/AKT Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Acidosis promotes cell apoptosis through the G protein-coupled receptor 4/CCAAT/enhancer-binding protein homologous protein pathway.Oncology letters · 2018Article
- Blocking Properdin Prevents Complement-Mediated Hemolytic Uremic Syndrome and Systemic Thrombophilia.Journal of the American Society of Nephrology : JASN · 2018Article
- Complement factor H protects mice from ischemic acute kidney injury but is not critical for controlling complement activation by glomerular IgM.European journal of immunology · 2018Article
- The pathogenesis of diclofenac induced immunoallergic hepatitis in a canine model of liver injury.Oncotarget · 2017Article
- Stop adding insult to injury-identifying and managing risk factors for the progression of acute kidney injury in children.Pediatric nephrology (Berlin, Germany) · 2017Review
- Increase in complement iC3b is associated with anti-inflammatory cytokine expression during late pregnancy in mice.PloS one · 2017Article
- Distinct roles for the complement regulators factor H and Crry in protection of the kidney from injury.Kidney international · 2016Article
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Abstract
The murine cell surface protein Crry (complement receptor 1-related protein/gene y) is a key complement regulator with similar activities to human membrane cofactor protein (MCP) and decay-accelerating factor. MCP has a critical role in preventing complement-mediated tissue injury and its mutation has been implicated in several human kidney diseases. The study of Crry in mice has relevance to understanding MCP activity in human diseases; however, such efforts have been hampered by the embryonic lethality phenotype of Crry gene knockout. Here we used a conditional gene-targeting approach and deleted Crry from the mouse proximal tubular epithelial cells where Crry is prominently expressed. Absence of Crry from proximal tubular epithelial cells resulted in spontaneous C3 deposition on the basolateral surface but no apparent renal disease in unchallenged mice. However, mice deficient in Crry on proximal tubular epithelial cells developed exacerbated renal injury when subjected to renal ischemia-reperfusion, showing increased blood urea nitrogen levels, higher tubular injury scores, more tubular epithelial cell apoptosis, and inflammatory infiltrates. Renal ischemia-reperfusion injury in the Crry conditional knockout mice was prevented by blocking C3 and C5 activation using an anti-properdin or anti-C5 monoclonal antibody (mAb), respectively. Thus, Crry has a critical role in protecting proximal tubular epithelial cells during ischemia-reperfusion challenge. Our results highlight the latent risk for inflammatory kidney injury associated with defects in membrane complement regulators.
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