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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.
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.
