Skip to main content
Fig. 7 | Stem Cell Research & Therapy

Fig. 7

From: miR-10a rejuvenates aged human mesenchymal stem cells and improves heart function after myocardial infarction through KLF4

Fig. 7

miR-10a overexpression or KLF4 downregulation increased old hBM-MSC survival and decreased apoptosis by activating AKT. miR-10a-overexpressed or KLF4-downregulated old hBM-MSCs (3 × 105 cells/mouse) implanted into infarcted mouse hearts. Cell survival and biochemical changes determined in mice that received implantation of control vector-transduced young hBM-MSCs (Y-c), control vector-transduced old hBM-MSCs (O-c), miR-10a-overexpressed old hBM-MSCs (O-10a), or KLF4-inhibited old hBM-MSCs (O-antiKLF4) into border region immediately following MI. Survival of implanted cells detected by green fluorescent protein (GFP) expression carried by lentiviral vector in border region of infarcted mouse hearts and cell apoptosis assayed by TUNEL staining at 3 days (a, b) and 7 days (c, d) post MI. e Expression of total AKT and phospho-(ser473)-AKT detected in border region of infarcted mouse hearts tissue. f Expression of phosphor-(ser473)-AKT also detected in hBM-MSCs. n = 6/group. Mean ± SD. *P < 0.05, Y-c vs other groups; #P < 0.05, O-c vs other groups. DAPI 4′,6-diamidino-2-phenylindole, hBM-MSC human mesenchymal stem cell, KLF4 Krüpple-like factor 4, MI myocardial infarction, TUNEL terminal deoxynucleotidyl transferase dUTP nick end labeling

Back to article page