*3.3. The Antifibrotic E*ff*ect was Not Accompanied by A Reduction of Myofibroblasts*

Despite interindividual differences within the control- and fibrocyte-ablated group, the overall hepatic expression of α-SMA was comparable both on protein- (Figure 3a,b) and transcriptional level (fold-change 1.08; 95% CI: 0.80–1.44; *p* = 0.614; Figure 3c). Immunohistochemical staining (Figure 3b), furthermore, revealed a similar staining intensity and distribution pattern of α-SMA. Additionally, we investigated the gene expression of the most potent myofibroblast activators TGF-β and PDGF. Both were expressed about equally in the control and the fibrocyte-ablated group (fold-change 1.16 and 0.99; *p* = 0.165 and 0.951; Figure 3c, full data in Figure S5a–c).

**Figure 3.** The antifibrotic effect was not accompanied by a reduction of myofibroblasts. (**a**) Western blot analysis and optical densitometry thereof revealed that the hepatic α-SMA levels were increased following TAA-treatment but unchanged by fibrocyte ablation. Two individual western blots were included in the analysis, a representative blot is shown. Arbitrary unit. *SC n* = 2; *Ctrl, FC-Abl. n* = 6. Mean + SEM is depicted. (**b**) Immunohistochemical staining of α-SMA (brown) demonstrated the periportal accumulation of myofibroblasts in TAA-treated animals and an unchanged expression pattern in result of the fibrocyte ablation. Representative stainings are shown. Magnification 40× and 200×, bars 400 and 50 μm. (**c**) Hepatic gene expression levels of *Acta2*, *Tgfb,* and *Pdgfb* were comparable at the end of the experiment (full data in Figure S5a–c).
