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Fig. 13 | Stem Cell Research & Therapy

Fig. 13

From: Mesenchymal stem cells ameliorate renal fibrosis by galectin-3/Akt/GSK3β/Snail signaling pathway in adenine-induced nephropathy rat

Fig. 13

The possible mechanism of MSCs against TGF-β1-induced fibrosis in Gal-3 KD HK-2 cells. In control groups, TGF-β1 induced the obvious increases in Gal-3 (A), α-SMA (B), KIM-1 (C), Snail (D), p-Akt (Ser473) (E), p-GSK3β (Ser9) (F), the ratio of TIMP1/MMP9 (G), and FN (H) compared with the normal group. MSCs-CM treatment notably decreased the expressions of above indexes after TGF-β1 treatment or only MSCs-CM without TGF-β1 treatment. DMEM/F12 medium treatment with no serum significantly upregulated these indexes compared with the TGF-β1+MSCs-CM group, especially the expression of KIM-1 and the ratio of p-GSK3β/GSK3β more than TGF-β1 group. In Gal-3 KD groups, the trends of each group were similar to those of the control groups, but lower than the same subgroup in control cells. DMEM/F12 treatment also resulted in obvious increases of aforementioned indexes compared with the TGF-β1+MSCs-CM group, but the expression of KIM-1 lower than the TGF-β1 group, and the ratio of p-GSK3β/GSK3β close to the TGF-β1 group. Results were normalized relative to the expression of β-actin. N = 3 (per group). Data are presented as mean ± SD, and analyzed by two-way ANOVA followed by Tukey post hoc testing. *P < 0.05, vs. control group, #P < 0.05, vs. TGF-β1+MSCs-CM group, &P < 0.05, vs. TGF-β1 +DMEM/F12 group, ^P < 0.05, vs. MSCs-CM group; compared empty transfection HK-2 cells with Gal-3 KD HK-2 cells, aP < 0.05, vs. normal group, bP < 0.05, vs. TGF-β1 group , cP < 0.05, vs. TGF-β1+MSCs -CM group, dP < 0.05, vs. TGF-β1+MSCs-CM group, eP < 0.05, vs. MSCs-CM group

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