Open AccessProtective effect of GDNF ‐engineered amniotic fluid‐derived stem cells on the renal ischaemia reperfusion injury in vitro
Author(s) -
Wang Jia,
Wang Fengzhen,
Wang Zhuojun,
Li Shulin,
Chen Lu,
Liu Caixia,
Sun Dong
Publication year - 2018
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12400
Subject(s) - glial cell line derived neurotrophic factor , neurotrophic factors , oxidative stress , stem cell , apoptosis , microbiology and biotechnology , superoxide dismutase , biology , chemistry , endocrinology , biochemistry , receptor
Objectives Amniotic fluid‐derived stem cells ( AFSC s) possessing multilineage differentiation potential are proposed as a novel and accessible source for cell‐based therapy and tissue regeneration. Glial‐derived neurotrophic factor ( GDNF ) has been hypothesized to promote the therapeutic effect of AFSC s on markedly ameliorating renal dysfunction. The aim of this study was to investigate whether AFSC s equipped with GDNF ( GDNF ‐ AFSC s) had capabilities of attenuating mouse renal tubular epithelial cells ( mRTEC s) apoptosis and evaluate its potential mechanisms. Materials and methods A hypoxia‐reoxygenation (H/R) model of the mRTEC s was established. Injured mRTEC s were co‐cultured with GDNF ‐ AFSC s in a transwell system. The mRNA expressions of hepatocytes growth factor ( HGF ) and fibroblast growth factor ( bFGF ) were detected by qRT ‐ PCR . Changes of intracelluar reactive oxygen species ( ROS ) and the level of superoxide dismutase ( SOD ) and malondialdehyde ( MDA ) were examined. The expressions of nitrotyrosine, Gp91‐phox, Bax, and Bcl‐2 were determined by Western blotting. Cell apoptosis was assayed by flow cytometry, and caspase‐3 activity was monitored by caspase‐3 activity assay kit. Results Our study revealed that expression of growth factors was increased and oxidative stress was dramatically counteracted in GDNF ‐ AFSC s‐treated group. Furthermore, apoptosis induced by H/R injury was inhibited in mRTEC s by GDNF ‐ AFSC s. Conclusions These data indicated that GDNF ‐ AFSC s are beneficial to repairing damaged mRTEC s significantly in vitro, which suggests GDNF ‐ AFSC s provide new hopes of innovative interventions in different kidney disease.