In Vitro Liver Fibrosis Assays
Liver fibrosis is the excessive accumulation of extracellular matrix (ECM) proteins including collagen that occurs in most types of chronic liver diseases. The main causes of liver fibrosis include chronic HCV infection, alcohol abuse, and nonalcoholic steatohepatitis (NASH). Activated hepatic stellate cells, portal fibroblasts, and myofibroblasts of bone marrow origin have been identified as major collagen-producing cells in the injured liver. These cells are activated by fibrogenic cytokines such as TGF-β1, angiotensin II, and leptin. Emerging antifibrotic therapies are aimed at inhibiting the accumulation of fibrogenic cells and/or preventing the deposition of extracellular matrix proteins.
Primary Adult Human Hepatic Stellate Cells (Normal & NASH)
TGFb-dependent fibrogenic gene induction (qRT-PCR, IF)
High throughput screen available
Figure 1
Figure 1. Human Hepatic Stellate Cells from a NASH patient and a healthy donor were cultured for 2 days post thaw, and harvested for qRT-PCR analysis. The fibrogenic genes are upregulated in NASH cells compared to normal cells. n=3. Error Bar: StdEV.
Figure 2
Figure 2. Human Hepatic Stellate Cells from the healthy donor were seeded on 6-well plates for transcriptomic analysis (A) or on 8-well chamber slides for immunofluorescence staining analysis (B). Prior to TGFb stimulation, cells were incubated with ALK5 Inhibitor (LY2157299) for 30 minutes followed by stimulation for 24h with 2.5 ng/ml TGFb.
Figure 3
Figure 3. Human Hepatic Stellate Cells from the NASH patient were seeded on 6-well plates for transcriptomic analysis (A) or 8-well chamber slides for immunofluorescence staining analysis (B). Cells were treated with or without ALK5 inhibitor (LY2157299), and harvested 24hr post treatment.
