Fig. 2

Airn deficiency aggravated CCl₄-induced liver fibrosis and LSEC capillarization in vivo. C57BL/6 mice were divided into four groups: WT (n = 10), WT + CCl₄ (n = 10), Airn-KO (n = 10), and Airn-KO +CCl₄ (n = 10). A Liver fibrosis was evaluated by macroscopic examination, H&E staining, sirius red staining, and IHC for α-SMA, COL1α1, and PCNA; scale bar, 400 μm for 10× and 100 μm for 40×. Right, five images of each liver and five livers from different mice were quantified for each group. B The protein level of α-SMA, COL1α1, MMP2, and TIMP1 was determined by western blot and quantitatively compared with GAPDH as a reference control. C The mRNA level of the genes related to liver fibrosis including α-SMA, Col1α1, Mmp2, and Timp1, and LSEC capillarization markers Cd31 and Laminin was determined by qRT-PCR. D Liver sections from CCl₄-induced fibrotic liver were analyzed using SEM and the protein level of CD31 and LAMININ staining was detected by IHC and quantitatively compared; scale bar, 400 μm for 10× and 100 μm for 40×. Data were quantified from 10 random fields per group for SEM, *p<0.05 stands for WT + CCl₄ or Airn-KO vs WT. #p<0.05 stands for Airn-KO + CCl₄ vs WT + CCl₄