ADRIANA REGINA MIRANDA
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Artigo IPEN-doc 16101 Immobilized kidney 28 KDa endostatin-related (KES28KDa) fragment promotes endothelial cell survival2010 - BELLINI, MARIA H.; MALPIGHI, THIAGO F.; CALVO, FERNANDA B.; MIRANDA, ADRIANA R.; SPENCER, PATRICK J.; CICHY, MILENA C.; SIMONS, SIMONE M.; TAVASSI, ANA M.C.; SANTOS, MARINILCE F. dos; RODRIGUES, CONSUELO J.; SCHOR, NESTORBackground/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 g (p ! 0.05); 12.5 versus 3.15 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.Artigo IPEN-doc 16097 Study of blood porphyrin spectral profile for diagnosis of chronic renal failure2010 - TRISTAO, VIVIAN R.; CARVALHO, FERNANDO F. de; GOMES, CINTHIA Z.; MIRANDA, ADRIANA R.; VEQUI-SUPLICY, CINTIA C.; LAMY, MARIA T.; SCHOR, NESTOR; BELLINI, MARIA H.The progression to end-stage renal failure is independent of the initial pathogenic mechanism. Metabolic acidosis is a common consequence of chronic renal failure that results from inadequate ammonium excretion and decreased tubular bicarbonate reabsorption. Protoporphyrin IX (PpIX) is the immediate metabolic precursor of the heme molecule. The purpose of this study was to evaluate the levels of erythrocytes protoporphyrin IX at an animal model during progressive renal disease. A total of 36 eightweek-old male Wistar rats were divided into six groups: Normal, 4 and 8 weeks after 5/6 nephrectomy (NX). Renal function was evaluated by creatinine clearance and plasma creatinine levels. The autofluorescence of erythrocytes porphyrin of healthy and NX rats was analyzed using fluorescence spectroscopy. Emission spectra were obtained by exciting the samples at 405 nm. Significant differences between normal and NX rats autofluorescence shape occurred in the 600ā700 nm spectral region. A correlation was observed between emission band intensity at 635 nm and progression of renal disease.