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10.1038/srep22111

http://scihub22266oqcxt.onion/10.1038/srep22111
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C4766468!4766468!26911791
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suck abstract from ncbi


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pmid26911791      Sci+Rep 2016 ; 6 (ä): ä
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  • The Synthetic Tie2 Agonist Peptide Vasculotide Protects Renal Vascular Barrier Function In Experimental Acute Kidney Injury #MMPMID26911791
  • Rübig E; Stypmann J; Van Slyke P; Dumont DJ; Spieker T; Buscher K; Reuter S; Goerge T; Pavenstädt H; Kümpers P
  • Sci Rep 2016[]; 6 (ä): ä PMID26911791show ga
  • Microvascular barrier dysfunction plays a major role in the pathophysiology of acute kidney injury (AKI). Angiopoietin-1, the natural agonist ligand for the endothelial-specific Tie2 receptor, is a non-redundant endothelial survival and vascular stabilization factor. Here we evaluate the efficacy of a polyethylene glycol-clustered Tie2 agonist peptide, vasculotide (VT), to protect against endothelial-cell activation with subsequent microvascular dysfunction in a murine model of ischemic AKI. Renal ischemia reperfusion injury (IRI) was induced by clamping of the renal arteries for 35?minutes. Mice were treated with VT or PEGylated cysteine before IRI. Sham-operated animals served as time-matched controls. Treatment with VT significantly reduced transcapillary albumin flux and renal tissue edema after IRI. The protective effects of VT were associated with activation of Tie2 and stabilization of its downstream effector, VE-cadherin in renal vasculature. VT abolished the decline in renal tissue blood flow, attenuated the increase of serum creatinine and blood urea nitrogen after IRI, improved recovery of renal function and markedly reduced mortality compared to PEG [HR 0.14 (95% CI 0.05?0.78) P?
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