Fig 2: Schematic representation of the effect of PM10 in EMT. PM10 exposure cause overexpression of TGFB1 in A549 cells, promoting the autoinduction of TGF-β signaling. As a result, SNAI1 (Snail), SNAI2 (Slug), ZEB1 (ZEB1), CDH2 (N-cadherin), ACTA2 (α-SMA), and VIM (vimentin) genes are overexpressed, while CDH1 (E-cadherin) is downregulated in a TGFB1-dependent way. PM10 also induces phosphorylation of SMAD2/3 and an increase in protein levels of SMAD4 in a TGFB1-independent way. These alterations predispose cells to the acquisition of an invasive phenotype, as evidenced by the invasion assay. Stop signal (in CDH1) represents gene repression, while green and red arrows represent increase and decrease of protein levels, respectively.

Fig 3: Inhibition of miR-183-5p alleviated liver fibrosis after bile duct ligation. (A) The expression of miR-183-5p was examined by RT-qPCR. (B) H&E and Masson staining of liver tissues in each group. 200×, Scale bar = 50 μm. (C) The quantification of Masson-positive fibrosis areas in each group. (D) Statistical quantification analysis showed the liver fibrosis score based on the Ishak scoring system. (E) TBIL level was measured by automatic chemiluminescence immunoassays (Roche Diagnostics). (F) ALT and AST levels was measured by automatic chemiluminescence immunoassays (Roche Diagnostics). (G,H) The protein levels of a-SMA, Collagen-I, and TIMP-1 were examined by western blotting. (I) Immunohistochemical staining of a-SMA in rat liver tissues. 200×, Scale bar = 50 μm. (J) The quantification of the a-SMA-positive area in each group. Data are expressed as the mean ± SD. n = 5 per group. *p < 0.05 vs. control antagomir Sham group, #P < 0.05 vs. control antagomir BDL group, ^p > 0.05 vs. control antagomir Sham group, ■ P > 0.05 vs. control antagomir BDL group, one-way ANOVA.

Fig 4: IL11 drives pancreatic stellate cell activation via ERK signalling and post-transcriptional effects. (a) RNA expression of IL11, ACTA2, COL1A1 and TIMP1 in PSCs treated with recombinant human TGFβ1 or IL11 (5 ng/mL; 24 h). (b) Representative immunofluorescence images and quantification of αSMA+ve cells, Collagen I intensity/area and EdU+ve cells at baseline and after 24 h treatment with IL11 (5 ng/mL) and ERK inhibitor U0126 (10 µM). Data are represented as mean ± SD in panel (a) and as median and whiskers extending from minimum to maximum values in panel (b). Scale bars: 100 µm. p values were determined by one way ANOVA (Dunnet’s correction) in (a) and one way ANOVA (Tukey’s correction) in (b). BL: baseline.

Fig 5: Renal histological changes and gene and protein expressions of fibrotic and angiogenic markers. a Representative micrographs of hematoxylin-eosin and Masson’s trichrome demonstrate histological changes in the 7 days post-surgery groups. Bar = 20 μm. b, c Quantification of renal interstitium areas in each group on both 3 and 7 days post-surgery (*P < 0.05, **P < 0.01, ***P < 0.001). d–h TGF-β1, a-SMA, and VEGF expression were confirmed after GDNF-AMSC treatment. Representative western blot (d) and quantitative data for TGF-β1 (e), a-SMA (g), and VEGF (h) are presented, and TGF-β1 mRNA levels were shown by real-time PCR (f) (*P < 0.05, **P < 0.01, ***P < 0.001)