Abstract
Activated hepatic stellate cells (HSC) play a central role in scar formation that leads to liver fibrosis. The molecular mechanisms underlying this process are not fully understood. Microarray and bioinformatics analyses have proven to be useful in identifying transcription factors that regulate cellular processes such as cell differentiation. Using oligonucleotide microarrays, we performed transcriptional analyses of activated human HSC cultured on Matrigel-coated tissue culture dishes. Examination of microarray data following Matrigel-induced deactivation of HSC revealed a significant down-regulation of myocardin, an important transcriptional regulator in smooth and cardiac muscle development. Thus, gene expression profiling as well as functional assays of activated HSC have provided the first evidence of the involvement of myocardin in HSC activation.
Highlights
Liver fibrosis is commonly observed after chronic liver injury and is believed to be a risk factor for cirrhosis and hepatocellular carcinomas (HCC)
Studies to date have demonstrated that several transcription factors, including KLF6 [4], cMyb [5], Smad3 [6], MEF2 [7], FOXO1 [8], and PPARδ [9] are involved in Hepatic stellate cells (HSC) activation
These results clearly underline the usefulness of transcriptional analysis of activated HSC in categorizing molecular mechanisms responsible for liver fibrosis
Summary
Liver fibrosis is commonly observed after chronic liver injury and is believed to be a risk factor for cirrhosis and hepatocellular carcinomas (HCC). Fibrosis is a disease typified by the increased production and decreased degradation of extracellular matrix (ECM) surrounding hepatocytes [1,2]. Hepatic stellate cells (HSC) is play a key role in disease progression [3]. Quiescent vitamin A-containing HSC are activated and assume a myofibroblast-like phenotype characterized by proliferation, contractility and chemotaxis, accompanied by a progressive loss of stored vitamin A. Activated HSC are trans-differentiate into a-smooth muscle actin (a-SMA)positive, and produce excessive ECM, including type I collagen and fibronectin. Studies to date have demonstrated that several transcription factors, including KLF6 [4], cMyb [5], Smad3 [6], MEF2 [7], FOXO1 [8], and PPARδ [9] are involved in HSC activation
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