Tissue Inhibitor of Metalloproteinases-2 Mediates Kidney Injury during Sepsis

descriptionPublicationkeyboard_double_arrow_right Article 01 Jan 2020 English Publisher:S. Karger AGJournal:Nephron, volume 144, pages 644-649 (issn: 1660-8151, eissn: 2235-3186,

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Authors: Xiaoyan, Wen; Jicheng, Zhang; Xiaojian, Wan; Alicia A, Frank; Xin, Qu; John A, Kellum;

doi: 10.1159/000511165

pmid: 33091916

Tissue Inhibitor of Metalloproteinases-2 Mediates Kidney Injury during Sepsis

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Abstract

Introduction: Urinary tissue inhibitor of metalloproteinases (TIMP)-2 has been identified as a predictive marker for acute kidney injury (AKI), including sepsis-associated AKI (S-AKI). Whether TIMP-2 might be causally related to AKI and hence represent a viable drug target is unclear. Objective: The aim of this study was to evaluate whether suppression of TIMP-2 attenuates S-AKI. Methods: Balb/c mice were randomized to sham or cecal ligation and puncture surgery and treated with or without a TIMP-2-neutralizing antibody. Animals were followed for 48 h and then sacrificed for analysis of TIMP-2 expression, cell cycle, and histology. Results: Anti-TIMP-2 resulted in decreased lumen TIMP-2 expression which markedly increased cell cycle progression and attenuated epithelial cell injury by histology. Conclusions: TIMP-2 mediates S-AKI and appears to be a viable drug target.

Related Organizations

University of Pittsburgh
United States

Keywords

Mice, Inbred BALB C, Tissue Inhibitor of Metalloproteinase-2, Cell Cycle, Epithelial Cells, Acute Kidney Injury, Flow Cytometry, Mice, Sepsis, Animals, Humans, Aged

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