Journal: International journal of molecular sciences

Article Title: The Dual-Mode Transition of Myofibroblasts Derived from Hepatic Stellate Cells in Liver Fibrosis.

doi: 10.3390/ijms242015460

Figure Lengend Snippet: Figure 2. Negative correlation between α-SMA and COL1A1 expression in myofibroblasts derived from hepatic stellate cells. (A). Correlation between α-SMA and COL1A1 expression in mesenchyme cells; data from Omnibrowser database. (B). The mRNA expression of α-SMA in HSC-T6 cells treated with 5% rat liver fibrosis serum. (C) The mRNA expression of α-SMA and COL1A1 in HSC-T6- derived myofibroblasts in the presence of gradient TGF-β1. (D) The protein expression of p-Smad2/3, α-SMA, and COL1A1 in HSC-T6-derived myofibroblasts in the presence of gradient TGF-β1. (E) The expression of TGF-β1 (red), α-SMA (green), and COL1A1 (pink) in the fibrotic liver of the rat was labeled with fluorescent tricolor (scale bar, 50 µm). The data represent the mean ± S.D. of three independent experiments. t-tests were used for statistical analysis. * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: The PVDF membranes were blocked with 5% skim milk in TBS and then incubated with primary antibodies at 4 ◦C for 12 h. The anti-α-SMA antibody (1:2000) was obtained from Proteintech (14395-1-AP, Rosemont, PA, USA).

Techniques: Expressing, Derivative Assay, Labeling

Journal: International journal of molecular sciences

Article Title: The Dual-Mode Transition of Myofibroblasts Derived from Hepatic Stellate Cells in Liver Fibrosis.

doi: 10.3390/ijms242015460

Figure Lengend Snippet: Figure 3. The dual mode transition of myofibroblasts derived from hepatic stellate cells (DMTM model). (A) In the DMTM model, myofibroblasts have dual modes. Myofibroblasts obtain high expression of α-SMA and enhanced tension, accompanied by inhibition of COL1A1 expression in the high-concentration region of TGF-β. At the edge of the TGF-β area, myofibroblasts convert to a high-collagen secretion phenotype. The DMTM model emphasizes the relationship between the TGF-β gradient and myofibroblast phenotype, which provides a more reasonable explanation for the formation of network collagen deposition. (B) In the traditional HSC activation model, myofi- broblasts simultaneously obtain high expression of α-SMA and COL1A1. Based on this model, the concentration gradient of TGF-β1 induces the activation of myofibroblasts in the high-concentration area and their quiescence in the low-concentration area. Activated myofibroblasts secrete collagen components, which leads to collagen deposition and clumping around TGF-β1-positive areas. Based on the traditional model, the tissue characteristics of the fibrotic liver will be the deposition of sheet- like fibers. However, this is inconsistent with the objective situation. (C) Model of the initiation and development of viral hepatitis and steatohepatitis-related liver fibrosis.

Article Snippet: The PVDF membranes were blocked with 5% skim milk in TBS and then incubated with primary antibodies at 4 ◦C for 12 h. The anti-α-SMA antibody (1:2000) was obtained from Proteintech (14395-1-AP, Rosemont, PA, USA).

Techniques: Derivative Assay, Expressing, Inhibition, Concentration Assay, Activation Assay