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Title: Immobilized Kidney 28-kDa Endostatin- Related (KES28kDa) Fragment Promotes Endothelial Cell Survival
Authors: Bellini, Maria Helena [UNIFESP]
Malpighi, Thiago Franca
Calvo, Fernanda Bernardes
Miranda, Adriana Regina
Spencer, Patrick Jack
Cichy, Milena Cristina [UNIFESP]
Simons, Simone Michaela
Chudzinski Tavassi, Ana Marisa
Santos, Marinilce Fagundes dos
Rodrigues, Consuelo Junqueira
Schor, Nestor [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Keywords: Acute kidney injury
Endothelial cell survival
Human umbilical vein endothelial cells
Issue Date: 1-Jan-2010
Publisher: Karger
Citation: American Journal of Nephrology. Basel: Karger, v. 31, n. 3, p. 255-261, 2010.
Abstract: Background/Objective: Renal ischemia-hypoxia is a leading cause of acute kidney injury (AKI). Ischemia causes extracellular matrix breakdown of the tubular basement membrane. Endostatin (ES) is the C-terminal fragment of collagen XVIII generated by proteolytic cleavage. Recent studies have demonstrated that ES expression is upregulated in ischemic kidneys. the present study aimed to characterize ES from ischemic kidneys. Methods: Ischemic renal failure was induced via 45 min of occlusion of the left renal artery and vein. After the ischemic period, blood was collected. Kidneys were harvested and used for immunohistochemical testing and protein extraction. Three-step purification was used. Soluble and immobilized purified ES were tested in cell viability and adhesion assays. Results: the soluble KES28kDa inhibited endothelial cell proliferation: 25 versus 12.5 mu g (p < 0.05); 12.5 versus 3.15 mu g (p < 0.05). Immobilization of KES28kDa supports endothelial cell survival over the control p = 0.021). Human umbilical vein endothelial cells plated on immobilized KES28kDa showed an increase in membrane ruffles and stress fibers. Conclusion: These data demonstrate the local synthesis of a 28-kDa ES-related fragment following AKI and suggest its role in endothelium survival. Copyright (C) 2010 S. Karger AG, Basel
ISSN: 0250-8095
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