Literature DB >> 23026513

Human umbilical cord blood-derived mesenchymal stem cells prevent diabetic renal injury through paracrine action.

Jong Hee Park1, Inah Hwang, Soo Han Hwang, Hoon Han, Hunjoo Ha.   

Abstract

AIMS: The present study examined renoprotective effect of human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSC) in diabetes. NRK-52E cells were utilized to determine the paracrine effect of hUCB-MSC.
METHODS: hUCB was harvested with the mother's consent. MSC obtained from the hUCB were injected through the tail vein. Growth arrested and synchronized NRK-52E cells were stimulated with transforming growth factor-β1 (TGF-β1) in the presence of hUCB-MSC conditioned media.
RESULTS: At 4 weeks after the streptozotocin (STZ) injection, diabetic rats showed significantly increased urinary protein excretion, renal and glomerular hypertrophy, fractional mesangial area, renal expression of TGF-β1 and α-smooth muscle actin, and collagen accumulation but decreased renal E-cadherin and bone morphogenic protein-7 expression, confirming diabetic renal injury. hUCB-MSC effectively prevented diabetic renal injury except renal and glomerular hypertrophy without a significant effect on blood glucose. CM-DiI-labeled hUCB-MSC and immunostaining of PKcs, a human nuclei antigen, confirmed a few engraftment of hUCB-MSC in diabetic kidneys. hUCB-MSC conditioned media inhibited TGF-β1-induced extracellular matrix upregulation and epithelial-to-mesenchymal transition in NRK-52E cells in a concentration-dependent manner.
CONCLUSIONS: These results demonstrate the renoprotective effect of hUCB-MSC in STZ-induced diabetic rats possibly through secretion of humoral factors and suggest hUCB-MSC as a possible treatment modality for diabetic renal injury.
Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

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Year:  2012        PMID: 23026513     DOI: 10.1016/j.diabres.2012.09.034

Source DB:  PubMed          Journal:  Diabetes Res Clin Pract        ISSN: 0168-8227            Impact factor:   5.602


  47 in total

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