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Lipocalin 2 Enhances Mesenchymal Stem Cell-Based Cell Therapy in Acute Kidney Injury Rat Model Publisher



Roudkenar MH1, 2 ; Halabian R3 ; Tehrani HA3 ; Amiri F4 ; Jahaniannajafabadi A5 ; Roushandeh AM6 ; Abbasimalati Z4 ; Kuwahara Y7
Authors
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Authors Affiliations
  1. 1. Department of Medical Biotechnology, Paramedicine Faculty, Guilan University of Medical Sciences, Rasht, Iran
  2. 2. Neuroscience Research Center, Guilan University of Medical Sciences, Rasht, Iran
  3. 3. Department of Medical Biotechnology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
  4. 4. Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tehran, Iran
  5. 5. Department of Pharmaceutical Biotechnology, and Isfahan Pharmaceutical Sciences Research Center, School of Pharmacy, Isfahan University of Medical Sciences and Health Services, Isfahan, Iran
  6. 6. Anatomical Sciences Department, Medicine Faculty, Hamadan University of Medical Sciences, Hamadan, Iran
  7. 7. Department of Radiation Biology and Medicine, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, 4-4-1, Komatsushima, Aoba-ku, Sendai, 981-8558, Miyagi, Japan

Source: Cytotechnology Published:2018


Abstract

Acute kidney injury (AKI) is one of the most common health-threatening diseases in the world. There is still no effective medical treatment for AKI. Recently, Mesenchymal stem cell (MSC)-based therapy has been proposed for treatment of AKI. However, the microenvironment of damaged kidney tissue is not favorable for survival of MSCs which would be used for therapeutic intervention. In this study, we genetically manipulated MSCs to up-regulate lipocalin-2 (Lcn2) and investigated whether the engineered MSCs (MSC-Lcn2) could improve cisplatin-induced AKI in a rat model. Our results revealed that up-regulation of Lcn2 in MSCs efficiently enhanced renal function. MSC Lcn2 up-regulates expression of HGF, IGF, FGF and VEGF growth factors. In addition, they reduced molecular biomarkers of kidney injury such as KIM-1 and Cystatin C, while increased the markers of proximal tubular epithelium such as AQP-1 and CK18 following cisplatin-induced AKI. Overall, here we over-expressed Lcn2, a well-known cytoprotective factor against acute ischemic renal injury, in MSCs. This not only potentiated beneficial roles of MSCs for cell therapy purposes but also suggested a new modality for treatment of AKI. © 2017, Springer Science+Business Media Dordrecht.
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