Additional file 1 of Exosomes derived from human adipose mesenchymal stem cells ameliorate hepatic fibrosis by inhibiting PI3K/Akt/mTOR pathway and remodeling choline metabolism

Additional file 1: Figure S1. Characterization of hADMSCs. Figure S2. TGF-β1 activates hepatic stellate cells leading to ECM deposition and EMT progression. Figure S3. Inhibition of activated HSCs proliferation and activation by hADMSCs. Figure S4. Liver cirrhosis was successfully induced in C57BL/6J mice with CCl4 i.p. injections twice a week for 8 weeks. Figure S5. Ex vivo organ distribution of PKH26-hADMSCs-Exo in CCl4-induced liver fibrosis mouse model. Figure S6. Liver stiffness of mouse with different treatments was measured by shear wave elastrography (SWE) at predetermined time. Figure S7. Representative histopathology analysis of liver sections after 0, 2 and 4 weeks of hADMSCs-Exo treatment. Figure S8. GO and KEGG pathway analyses between LFG vs hADMSCs-Exo or REG. Figure S9. Western blot assay for AKT, mTOR and phosphorylated and total PI3K p85 and PI3K p110 in vivo (A) and in vitro (B). Figure S10. The gene coding for the key metabolite expression analysis in transcriptome. Figure S11. Western blot assay for pro-fibrogenic and PI3K/AKT/mTOR signaling protein expression in aHSCs following supplementation with hADMSCs-Exo and 10 mM choline or 10 mM phosphorylcholine simultaneously in vitro. Table S1. Primer sequences used in reverse transcription quantitative PCR (RT-qPCR). Table S2. Antibodies utilized in Western blot, immunohistochemistry or Immunofluorescence staining. Table S3. The top 25 significant KEGG pathway between hADMSCs-Exo group (n=3) and regression group (REG, n=3). Table S4. Significant metabolites between hADMSCs-Exo treatment group (n=6) and regression group (n=6) in the liver tissue samples. Table S5. Significant metabolites between hADMSCs-Exo treatment group (n=6) and liver fibrosis group (n=6) in the liver tissue samples.