Fig 1: MiR-21 rescued the inhibition function of Gas5. a Cell proliferation of HCS-2/8 gene function models assessed by MTT assays. b The expression of FGF1 and active caspase 9 proteins were assessed by western blot assays. c Cell apoptosis analysis was quantified by Annexin V-FITC assay and fluorescence flow cytometry. d Cell cycle analysis was quantified by PI staining and fluorescence flow cytometry
Fig 2: (A) There was enhanced immunoreactivity for FGF1 (red) in cholangiocytes (blue) in liver sections co‐stained with CK‐19 from Mdr2 −/− mice, and immunoreactivity that was decreased by treatment with AZD4547; no immunoreactivity for FGF1 was observed for HSCs in liver sections co‐stained with desmin (green). Scale bar = 5 µm. (B,C) There was increased mRNA expression of FGF1 in cholangiocytes and higher FGF1 levels in serum from Mdr2 −/− mice compared with FVB/NJ mice. Data are presented as mean ± SEM of four quantitative PCR reactions from three cumulative preparations of cholangiocytes from nine mice. Serum levels were measured in three samples from nine different animals. *P < 0.05 versus FVB/NJ mice; # P < 0.05 versus Mdr2 −/− mice.
Fig 3: Rat model assay. a Rat tibiae growth plate sections from the control group, the Dex-treated group or the Gas5 overexpression lentivirus-infected group were prepared for staining analysis: HE staining (100 ×) for growth plate chondrocytes, IHC staining for FGF1 (400 ×) and active caspase 9 (400 ×), fluorescence in situ hybridisation for miR-21 (200 ×). b The weight, tibiae length, nose-tail length and BALP expression analysis of rats from the control group, the Dex-treated group or the Gas5 overexpression lentivirus-infected group. Data are presented as mean ± s.d., n = 10. *p < 0.05 or **p < 0.01 vs. control group. (c) GAS5 and FGF1 expressions in Dex-treated and untreated chondrocytes
Fig 4: The regulation of Gas5 and miR-21 in cell apoptosis and cell cycle of HCS-2/8 cells treated with or without Dex. a Cell apoptosis analysis was quantified by Annexin V-FITC assay and fluorescence flow cytometry. b Cell cycle analysis was quantified by PI staining and fluorescence flow cytometry. c The expression of FGF1 and active caspase 9 proteins were assessed by western blot assays. d Cellular apoptosis analysis was quantified by Annexin V-FITC assay and fluorescence flow cytometry. e Cell cycle analysis was quantified by PI staining and fluorescence flow cytometry. Data are presented as mean ± s.d., n = 3. *p < 0.05 or **p < 0.01 vs. Scramble group. #p < 0.05 or ##p < 0.01 vs. Scramble+Dex group
Fig 5: Correlation of miR‐210‐3p expression with hypoxia‐inducible factor 1α (HIF1α) and fibroblast growth factor 1 (FGF1) expression in placental tissues. A, qRT‐PCR analysis of the relative expression of miR‐210‐3p in placental tissues from eight pairs of selective intrauterine growth restriction (sIUGR) twins (P1‐P8). B, Western blotting analysis of the protein levels of FGF1 and HIF1α in placental tissues from eight pairs of sIUGR twins (P1‐P8). C, Correlation analysis of miR‐210‐3p expression with FGF1 and HIF1α expression. L, larger twin; S, smaller twin. (*P < 0.05, **P < 0.01)
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