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Exogenous pentraxin-3 inhibits the reactive oxygen species-mitochondrial and apoptosis pathway in acute kidney injury

Authors
 Hyung Ho Lee  ;  Sook Young Kim  ;  Joon Chae Na  ;  Young Eun Yoon  ;  Woong Kyu Han 
Citation
 PLoS One, Vol.13(4) : e0195758, 2018 
Journal Title
 PLoS One 
Issue Date
2018
MeSH
Acute Kidney Injury/*metabolism/pathology ; Apoptosis/drug effects ; C-Reactive Protein/*pharmacology ; Cell Line ; Cell Survival/drug effects ; Humans ; Hypoxia/drug therapy/metabolism ; Ischemia/drug therapy/metabolism ; Matrix Metalloproteinases ; Mitochondria/*drug effects/*metabolism ; Protective Agents/pharmacology ; Reactive Oxygen Species/*metabolism ; Serum Amyloid P-Component/*pharmacology
Abstract
Pentraxin-3 (PTX3) is a long-form member of the pentraxin family of proteins that has been studied in inflammatory diseases and in various organs. We found that PTX3 protects kidney cells during ischemia and proinflammatory acute kidney injury. The aim of this study was to develop an in vitro experimental model of acute kidney injury and to analyze the protective mechanism of exogenous recombinant PTX3. In this study, cells of the HK-2 renal tubular cell line were treated with a calcium ionophore (A23187), which induced injury by increasing intracellular calcium concentrations and inducing calpain activity and the generation of reactive oxygen species. Exposure of cells to PTX3 significantly attenuated these effects. In addition, the activity of caspase-3 and PARP-1 were decreased in ischemic cells exposed to exogenous recombinant PTX3. PTX3 stabilized the mitochondrial membrane potential and suppressed apoptosis, resulting in the protection of renal tubular cells from ischemic injury.
Files in This Item:
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DOI
10.1371/journal.pone.0195758
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Urology (비뇨의학교실) > 1. Journal Papers
Yonsei Authors
Na, Joon Chae(나준채) ORCID logo https://orcid.org/0000-0003-4449-8472
Yoon, Young Eun(윤영은)
Lee, Hyung Ho(이형호)
Han, Woong Kyu(한웅규) ORCID logo https://orcid.org/0000-0002-2527-4046
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/162287
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