Fig. 7

BMSCs regulate the IL7R/JAK1/STAT5 pathway in HSCs by modulating the secretion of IL7 by hepatic cells. (A) Microscopic images of each group stained with HE, Masson, Sirius Red, ACTA2, p-STAT5 and STAT5 (magnification: ×100, n = 6). Area stained with Masson, Sirius Red, ACTA2, and p-STAT5/STAT5, as well as Metavir fibrosis staging. The levels of serum ALT, AST, and TBil in each group. (B) Western blot analyses of COL1A1, JAK1, p-STAT5, STAT5 and ACTA2 in liver tissue. TUBA1A was used as the loading control except for p-STAT5. STAT5 was used as the loading control for p-STAT5. Col1a1, Jak1, and Acta2 mRNA levels in liver tissue. (C) Western blot analyses of IL7 in IAR20 cells. TUBA1A was used as the loading control. Il7 mRNA levels in IAR20 cells. (D) Western blot analyses of COL1A1, JAK1, p-STAT5, STAT5 and ACTA2 in HSC-T6 cells. TUBA1A was used as the loading control except for p-STAT5. STAT5 was used as the loading control for p-STAT5. Col1a1, Jak1 and Acta2 mRNA levels in HSC- T6 cells. Full-length blots/gels are presented in Supplementary Fig. 6. The samples were derived from the same experiment and processed in parallel. ACTA2, actin alpha 2; ALT, alanine aminotransferase; AST, aspartate aminotransferase; BMSCs, bone mesenchymal stem cells; COL1A1, collagen type I alpha 1 chain; IL, interleukin; JAK, Janus-activated kinase; LT, liver transplantation; STAT, signal transducer and activator of transcription; TBil, total bilirubin. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001