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Properdin Deficiency Impairs Phagocytosis and Enhances Injury at Kidney Repair Phase Post Ischemia-Reperfusion.
Wu, Yuanyuan; Zwaini, Zinah D; Brunskill, Nigel J; Zhang, Xinyue; Wang, Hui; Chana, Ravinder; Stover, Cordula M; Yang, Bin.
Afiliación
  • Wu Y; Department of Cardiovascular Sciences, College of Life Sciences, University of Leicester, University Hospitals of Leicester NHS Trust, Leicester, United Kingdom.
  • Zwaini ZD; Basic Medical Research Centre, Medical School of Nantong University, Nantong, China.
  • Brunskill NJ; Department of Respiratory Sciences, College of Life Sciences, University of Leicester, Leicester, United Kingdom.
  • Zhang X; Department of Cardiovascular Sciences, College of Life Sciences, University of Leicester, University Hospitals of Leicester NHS Trust, Leicester, United Kingdom.
  • Wang H; Nantong-Leicester Joint Institute of Kidney Science, Department of Nephrology, Affiliated Hospital of Nantong University, Nantong, China.
  • Chana R; Department of Cardiovascular Sciences, College of Life Sciences, University of Leicester, University Hospitals of Leicester NHS Trust, Leicester, United Kingdom.
  • Stover CM; Nantong-Leicester Joint Institute of Kidney Science, Department of Nephrology, Affiliated Hospital of Nantong University, Nantong, China.
  • Yang B; Department of Respiratory Sciences, College of Life Sciences, University of Leicester, Leicester, United Kingdom.
Front Immunol ; 12: 697760, 2021.
Article en En | MEDLINE | ID: mdl-34552582
ABSTRACT
Properdin, a positive regulator of complement alternative pathway, participates in renal ischemia-reperfusion (IR) injury and also acts as a pattern-recognition molecule affecting apoptotic T-cell clearance. However, the role of properdin in tubular epithelial cells (TECs) at the repair phase post IR injury is not well defined. This study revealed that properdin knockout (PKO) mice exhibited greater injury in renal function and histology than wild-type (WT) mice post 72-h IR, with more apoptotic cells and macrophages in tubular lumina, increased active caspase-3 and HMGB1, but better histological structure at 24 h. Raised erythropoietin receptor by IR was furthered by PKO and positively correlated with injury and repair markers. Properdin in WT kidneys was also upregulated by IR, while H2O2-increased properdin in TECs was reduced by its small-interfering RNA (siRNA), with raised HMGB1 and apoptosis. Moreover, the phagocytic ability of WT TECs, analyzed by pHrodo Escherichia coli bioparticles, was promoted by H2O2 but inhibited by PKO. These results were confirmed by counting phagocytosed H2O2-induced apoptotic TECs by in situ end labeling fragmented DNAs but not affected by additional serum with/without properdin. Taken together, PKO results in impaired phagocytosis at the repair phase post renal IR injury. Properdin locally produced by TECs plays crucial roles in optimizing damaged cells and regulating phagocytic ability of TECs to effectively clear apoptotic cells and reduce inflammation.
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Texto completo: 1 Colección: 01-internacional Asunto principal: Fagocitosis / Properdina / Daño por Reperfusión / Riñón Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Front Immunol Año: 2021 Tipo del documento: Article País de afiliación: Reino Unido

Texto completo: 1 Colección: 01-internacional Asunto principal: Fagocitosis / Properdina / Daño por Reperfusión / Riñón Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Front Immunol Año: 2021 Tipo del documento: Article País de afiliación: Reino Unido