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The Interplay of TGF-β1 and Cholesterol Orchestrating Hepatocyte Cell Fate…

- - - - defective hepatocyte regeneration for the replenishment of dead cells and the adverse factors, including inflammatory factors, dietary factors, and lipopolysaccharide, are the proposed hits that drive the progression of MASLD to fibrosis
        
        the activation of hepatic stellate cells (HSCs)
        
        accumulating collagen and extracellular matrix production/deposition and portal hypertension
  - - - cholesterol
        
        Fifty percent of total cholesterol biosynthesis in human beings occurs in the liver
        
        affects membrane fluidity and modulates membrane trafficking, host–pathogen interaction, and signal transduction
        
        TGF-β1 is a 25-kilodalton homodimeric peptide, playing significant roles in various biological processes
        
        TGF-βs signal through binding to plasma membrane complexes of type II (TβR-II) and type I (TβR-I) TGF-β receptors
      - free fatty acids
      - diacylglycerol
- - - - chord diagram
        
        etworking analysis shows that the majority of these genes display coexpression and colocalization
        
        Analysis of the signaling pathways shows that there also is notable down-regulation of genes involved in enhancing cholesterol esterification, bile acid signaling pathways, sterol regulatory element binding protein signaling pathway, and cellular response to cholesterol
  - - - RT-qPCR) in AML12 cells (control vs TGF-β1–treated)
        
        24-hour incubation with TGF-β1 had an inhibitory effect on messenger RNA (mRNA) expression of Hmgcr and Sqle compared with the control group
        
        Protein expression of HMGCR in the liver tissue of control or AAV8–TGF-β1 mice was determined by Western blot
        
        Total cholesterol concentration was examined in the liver tissue of mice treated with AAV8–control or AAV8–TGF-β1.
        
        Lipid droplet accumulation in liver tissue of mice treated with AAV8–control or AAV8–TGF-β1 was examined by BODIPY staining.
  - - - AML12 cells treated for CE, CD, or untreated (control) then were stimulated with 2 ng/mL TGF-β1 for 2 hours.
        
        Cells treated to alter their cholesterol levels as described earlier were incubated with 2 ng/mL TGF-β1 for 30 minutes and subjected to Western blot of p-AKT and total AKT. For RT-qPCR,