Deletion of Mettl3 at the Pro-B Stage Marginally Affects B Cell Development and Profibrogenic Activity of B Cells in Liver Fibrosis

Figure 6

Knockout of Mettl3 does not affect the pro-fibrogenic activity of B cells in liver fibrosis. (a) Quantitation of mRNA expression level of Mettl3 in B cells isolated from mouse livers treated with CCl₄ or Oil (control) for 6 weeks. Results were retrieved from published microarray data [47]. (b) Schematic diagram of CCl₄-induced mouse liver fibrosis. (c, d) Quantification of flow cytometry analysis for B cell activation marker CD86 and CD95 in the spleen (c) and liver tissues (d) of WT control and Mettl3 cKO mice after fibrosis induction. (e) Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin (ALB), and alkaline phosphatase (ALP) levels in indicated groups 24 h after the last CCl₄ treatment ( for WT control and mice for Mettl3 cKO). (f) RT-qPCR for profibrogenic genes of liver tissues in indicated groups ( for WT control and for Mettl3 cKO). (g) Representative western blot (left) and quantification (right) for profibrogenic genes in indicated groups (/group). Gapdh was used as a loading control. (h) Representative photographs of H&E staining (left), αSMA immunohistochemistry staining (middle), and picrosirius red (PSR) staining (right) of fibrotic liver sections from WT control and Mettl3 cKO mice. (i, j) Quantification of the aSMA positive area (i) and PSR staining positive area (j) in indicated groups ( for WT control and for Mettl3 cKO). Data in (a), (c)–(f), and (i, j) were presented as with the indicated significance (; student’s -test).

(a)

(b)

(c)

(d)

(e)

(f)

(g)

(h)

(i)

(j)