Hepatic fibrosis is enhanced and accompanied by robust oval cell activation after chronic carbon tetrachloride administration to Egr-1-deficient mice.

摘要: The transcription factor early growth response (Egr)−1 regulates the expression of genes required for execution wound healing response. Multiple cycles injury, coupled to incomplete healing, lead fibrosis. Therefore, we hypothesized that Egr-1 is development hepatic To test this hypothesis, exposed wild-type and egr-1−/− mice acute or chronic carbon tetrachloride (CCl4). Acute CCl4 exposure established a profibrotic milieu in liver, including activation stellate cells as well type 1 collagen tissue inhibitor matrix metalloproteinase both mice. This was exacerbated After exposure, fibrosis genotypes; however, fibrotic profoundly worsened Egr-1–deficient Importantly, enhanced accompanied by robust oval cell response, suggesting more severe liver injury and/or reduced hepatocyte proliferation when compared with Hepatic indicative activation, number expressing A6, mouse marker, greater Taken together, these data reveal novel roles negative regulator CCl4-induced