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BioMed Research International
Volume 2013 (2013), Article ID 526367, 13 pages
http://dx.doi.org/10.1155/2013/526367
Research Article

Kidney-Targeted Transplantation of Mesenchymal Stem Cells by Ultrasound-Targeted Microbubble Destruction Promotes Kidney Repair in Diabetic Nephropathy Rats

1Department of Ultrasound, Xinqiao Hospital of the Third Military Medical University, 183 Xinqiaozheng Road, Chongqing 400037, China
2Department of Ultrasound, The Forty-Fourth Military Hospital, 67 Huanghe Road, Guiyang 550009, China
3Department of Orthopaedics, The Affiliated Hospital of Guiyang Medical College, 28 Guiyi Street, Guiyang 550004, China
4Center for Tissue Engineering and Stem Cells, Guiyang Medical College, 9 Beijing Road, Guiyang 550004, China

Received 3 March 2013; Revised 19 April 2013; Accepted 19 April 2013

Academic Editor: Ken-ichi Isobe

Copyright © 2013 Yi Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

We test the hypothesis that ultrasound-targeted microbubble destruction (UTMD) technique increases the renoprotective effect of kidney-targeted transplantation of bone-marrow-derived mesenchymal stem cells (BM-MSCs) in diabetic nephropathy (DN) rats. Diabetes was induced by streptozotocin injection (60 mg/Kg, intraperitoneally) in Sprague-Dawley rats. MSCs were administered alone or in combination with UTMD to DN rats at 4 weeks after diabetes onset. Random blood glucose concentrations were measured at 1, 2, 4, and 8 weeks, and plasma insulin levels, urinary albumin excretion rate (UAER) values, the structures of pancreas and kidney, the expressions of TGF-β1, synaptopodin, and IL-10 were assessed at 8 weeks after MSCs transplantation. MSCs transplantation decreased blood glucose concentrations and attenuated pancreatic islets/β cells damage. The permeability of renal interstitial capillaries and VCAM-1 expression increased after UTMD, which enhanced homing and retention of MSCs to kidneys. MSCs transplantation together with UTMD prevented renal damage and decreased UAER values by inhibiting TGF-β1 expression and upregulating synaptopodin and IL-10 expression. We conclude that MSCs transplantation reverts hyperglycemia; UTMD technique noninvasively increases the homing of MSCs to kidneys and promotes renal repair in DN rats. This noninvasive cell delivery method may be feasible and efficient as a novel approach for personal MSCs therapy to diabetic nephropathy.