Abstract

You have accessJournal of UrologyStem Cell Research1 Apr 2011184 AMNIOTIC FLUID STEM CELLS AND CHRONIC KIDNEY DISEASE Sargis Sedrakyan, Laura Perin, Stefano Da Sacco, Liron Shiri, Kevin Lemley, and Roger De Filippo Sargis SedrakyanSargis Sedrakyan Los Angeles, CA More articles by this author , Laura PerinLaura Perin Los Angeles, CA More articles by this author , Stefano Da SaccoStefano Da Sacco Los Angeles, CA More articles by this author , Liron ShiriLiron Shiri Los Angeles, CA More articles by this author , Kevin LemleyKevin Lemley Los Angeles, CA More articles by this author , and Roger De FilippoRoger De Filippo Los Angeles, CA More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2011.02.253AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Alport Disease, the model used in our experiments, is characterized by a hereditary form of glomerulonephritis, wherein an abnormal level of glomerular basement membrane (GBM) is produced, gradually leading to interstitial fibrosis and eventual loss of renal function. At present, there is no definitive therapy to delay progression of fibrosis, which is the hallmark in a majority of chronic kidney disease (CKD) cases. Stem-cell based therapies may provide alternative therapeutic opportunities. Amniotic fluid stem cells (AFSCs) are well established to have both pluripotential and paracrine functions and represent a possible alternative approach to current therapies for CKD. METHODS In this study we have applied AFSCs in an in vivo model of chronic Alport Disease. Intracardiac injections of AFSCs have been performed on Alport mice between 2 and 3 months after birth. Changes in BUN, creatinine levels and albuminuria have been compared between injected mice and not injected siblings. Real Time PCR and Western Blotting have been used to evaluate cytokine expression. Immunohistochemistry and immunofluorescence have been performed to follow morphological modifications, extracellular matrix deposition and cast formation. RESULTS Systemic injection of the cells provides beneficial effects; we found decreased levels of albuminuria, creatinine and BUN as well as significant increase in the life-span of the treated mice as compared to their untreated controls. Additionally, treated mice present lower number of macrophage infiltration, lower myofibrostast trasformation in the kidney interstitial space, accompanied with downregulated expression of chemokines such as MPC-1, IP-10 and cytokines such as IL-1, TNF-α and TGF-α. CONCLUSIONS In this study we have shown that AFSCs are capable of slowing down the progression of Alport disease by incurring structural and functional benefits to the kidney. These cells may present an alternative approach to treat various medical conditions where currently therapeutic options are either limited or inadequate. © 2011 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 185Issue 4SApril 2011Page: e76 Advertisement Copyright & Permissions© 2011 by American Urological Association Education and Research, Inc.MetricsAuthor Information Sargis Sedrakyan Los Angeles, CA More articles by this author Laura Perin Los Angeles, CA More articles by this author Stefano Da Sacco Los Angeles, CA More articles by this author Liron Shiri Los Angeles, CA More articles by this author Kevin Lemley Los Angeles, CA More articles by this author Roger De Filippo Los Angeles, CA More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

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