Bile acid stimulation of early growth response gene and mitogen-activated protein kinase is protein kinase C-dependent
| Autor: | David W.A. Beno, Bernard H. Davis, Lynda Brady |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Male
Taurocholic Acid medicine.medical_specialty Transcription Genetic Liver cytology medicine.drug_class Cholic Acid Biology Biochemistry Immediate-Early Proteins Bile Acids and Salts Rats Sprague-Dawley chemistry.chemical_compound Internal medicine medicine Animals Protein kinase A Molecular Biology Cells Cultured Protein Kinase C Protein kinase C Early Growth Response Protein 1 Bile acid Cholic acid Genes fos Cholic Acids Cell Biology G protein-coupled bile acid receptor Rats Cell biology DNA-Binding Proteins Enzyme Activation Isoenzymes Endocrinology Liver chemistry Calcium-Calmodulin-Dependent Protein Kinases Hepatic stellate cell Tetradecanoylphorbol Acetate Lithocholic Acid Hepatic fibrosis Transcription Factors Research Article |
| Zdroj: | Biochemical Journal. 316:765-769 |
| ISSN: | 1470-8728 0264-6021 |
| Popis: | Hepatic stellate cells are exposed to elevated bile acid levels during hepatic injury and fibrogenesis. Upon activation, the stellate cell becomes a major effector cell during the development of hepatic fibrosis and cirrhosis. Bile acids may function as co-stimulatory signalling molecules. This hypothesis was tested in vitro using rat-derived hepatic stellate cells. Bile acids were studied at concentrations that occur during cirrhosis in vivo. Conjugated and unconjugated bile acids rapidly induced egr and fos gene expression as well as cytoplasmic mitogen-activated protein kinase (MAPK) activation. Protein kinase C was required for both egr induction and MAPK activation. These studies imply that bile acids could contribute to the perpetuation of hepatic fibrosis by helping to keep the stellate cell in an activated state. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|