Enhanced renoprotective effect of IGF-1 modified human umbilical cord-derived mesenchymal stem cells on gentamicin-induced acute kidney injury

Sci Rep. 2016 Feb 2:6:20287. doi: 10.1038/srep20287.

Abstract

The therapeutic action of umbilical cord-derived mesenchymal stem cells (UC-MSCs) against acute kidney injury (AKI) has been demonstrated by several groups. However, how to further enhance the renoprotective effect of UC-MSCs and improve the therapy effect, are still unclear. In this study, we mainly investigated whether insulin-like growth factor-1 (IGF-1)-modified UC-MSCs hold an enhanced protective effect on gentamicin-induced AKI in vivo. Our results indicated that the IGF-1 overexpression could enhance the therapeutic action of human UC-MSCs, and the AKI rats treated with IGF-1-overexpressed UC-MSCs (UC-MSCs-IGF-1) showed better recovery of biochemical variables in serum or urine associated with renal function, histological injury and renal apoptosis, compared with AKI rats treated with normal UC-MSCs. RNA microarray analysis indicated that some key genes in the signal pathways associated with anti-oxidation, anti-inflammatory, and cell migratory capacity were up-regulated in UC-MSCs-IGF-1, and the results were further confirmed with qPCR. Furthermore, a series of detection in vitro and in vivo indicated that the UC-MSCs-IGF-1 hold better anti-oxidation, anti-inflammatory, and cell migratory capacity for IGF-1 overexpression. Thus, our study indicated that enhancement of UC-MSCs bioactivities with IGF-1 overexpression could increase the UC-MSCs therapeutic potential and further developed a new therapeutic strategy for the treatment of AKI.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Kidney Injury / chemically induced
  • Acute Kidney Injury / metabolism*
  • Acute Kidney Injury / pathology*
  • Acute Kidney Injury / therapy
  • Animals
  • Antigens, Surface / metabolism
  • Antioxidants / metabolism
  • Apoptosis / drug effects
  • Apoptosis / genetics
  • Biomarkers
  • Cell Movement / drug effects
  • Cell Movement / genetics
  • Cytokines / metabolism
  • Disease Models, Animal
  • Gene Expression
  • Gene Expression Profiling
  • Gentamicins / adverse effects
  • Humans
  • Immunophenotyping
  • Inflammation Mediators / metabolism
  • Insulin-Like Growth Factor I / genetics*
  • Insulin-Like Growth Factor I / metabolism
  • Mesenchymal Stem Cell Transplantation*
  • Mesenchymal Stem Cells / cytology*
  • Mesenchymal Stem Cells / metabolism*
  • Oxidation-Reduction
  • Rats
  • Umbilical Cord / cytology*

Substances

  • Antigens, Surface
  • Antioxidants
  • Biomarkers
  • Cytokines
  • Gentamicins
  • Inflammation Mediators
  • Insulin-Like Growth Factor I