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Fig. 7 | Stem Cell Research & Therapy

Fig. 7

From: Inhibition of miR-199a-5p rejuvenates aged mesenchymal stem cells derived from patients with idiopathic pulmonary fibrosis and improves their therapeutic efficacy in experimental pulmonary fibrosis

Fig. 7

Transplantation of anti-miR-199a-5p-IPF-MSCs attenuated fibrosis formation and inflammation in a mouse model of pulmonary fibrosis. a Western blotting analysis of collagen I and α-SMA expression in lung tissue from control group mice, bleomycin group mice, and bleomycin group mice that received control-MSCs, IPF-MSCs, or anti-miR-199a-5p-IPF-MSCs, respectively. b Measurement of the mRNA level of collagen I and α-SMA expression in the lung tissue from control group mice, bleomycin group mice, control-MSC group mice, IPF-MSC group mice, or anti-miR-199a-5p-IPF-MSCs group mice. c Measurement of mRNA level of proinflammatory genes in the lung tissue from control group mice, bleomycin group mice, control-MSC group mice, IPF-MSC group mice, or anti-miR-199a-5p-IPF-MSC group mice. d IPF-MSCs demonstrate increased cellular senescence and decreased therapeutic function. After inhibition by miR-199a-5p, the vitality of IPF-MSCs was restored by regulating autophagy level by activating Sirt1/AMPK signaling pathway. Anti-miR-199a-5p-IPF-MSCs had greater antifibrotic effects in a mouse model of pulmonary fibrosis induced by bleomycin than IPF-MSCs. Data represent the mean ± SEM from groups of six mice. *p < 0.05; **p < 0.01; ***p < 0.001

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