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. 2017 May 18;14(3):201–210. doi: 10.1007/s13770-017-0026-5

Table 2.

MSCs as Treatment of Podocyte Injury in DN

Source Experimental model Route of injection In vivo localization of MSCs  Mechanism of action Findings
AD-MSCs Mouse podocyte clone 5 cells (MPC5) _ _ Secretion of soluble epithelial growth factor AD-MSCs reduced podocytic apoptosis reduced the expression of podocytic cleaved caspase-3, maintained integrity of glomerular filtration barriers by increasing podocytic synaptopodin and nephrin expression [83]
SD rats + STZ and MPC5, n = 11 Intravenous Lung, spleen and a small number in kidney and pancreas Secretion of GDNF AD-MSCs attenuated proteinuria, prevented high glucose-induced podocyte injury and maintained the integrity of the podocyte actin cytoskeleton by increasing the expression of WT1 and synaptopodin proteins [92]
BM-MSCs SD rats + STZ,
n = 14
Intra-arterial  Kidney Increased BMP-7, nephrin and podocin secretion BM-MSCs ameliorated loss of podocytes, GBM thickening and podocyte foot process effacement. By restoration of expression of nephrin and podocin [94]
UC-MSCs Mouse podocyte clone 5 cell (MPC5) _ _ Secretion of soluble epithelial growth factor UC-MSCs decreased the podocytic apoptosis rate and the expression of PARP, increased the expression of Bcl-2, normalized the expression and arrangement of podocytic podoplanin [91]

MSCs Mesenchymal stem cells; AD-MSCs Adipose-derived mesenchymal stem cells; BM-MSCs Bone marrow mesenchymal stem cells; AD-MSCs Adipose-derived mesenchymal stem cells; UC-MSCs Umbilical cord mesenchymal stem cells; Sprague–Dawley (SD) rats; STZ Streptozotocin; GBM Glomerular basement membrane; GDNF Glial derived neurotrophic factor; WT1 Wilms tumor protein 1; Bcl-2 B cell lymphoma-2; PARP Poly ADP ribose polymerase