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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Antineoplastic Agents, Biological Transport, Cell Division, Cell Movement, Cell Survival, Cells, Cultured, Chemokine CCL2, Chromans, Cytotoxins, Gene Expression, Hepatitis, Humans, Interleukin-1, Ligands, Liver, Liver Cirrhosis, Mitogen-Activated Protein Kinases, NF-kappa B, Phosphorylation, Platelet-Derived Growth Factor, Prostaglandin D2, Proto-Oncogenes, RNA, Messenger, Receptors, Cytoplasmic and Nuclear, Thiazoles, Thiazolidinediones, Transcription Factor AP-1, Transcription Factors, Troglitazone, Tyrosine, Wound Healing, p38 Mitogen-Activated Protein Kinases.
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Do ligands of peroxisome proliferator-activated receptor gamma modulate profibrogenic and proinflammatory actions in hepatic stellate cells? Context: Proliferation and migration of hepatic stellate cells (HSCs) and expression of chemokines are involved in the pathogenesis of liver inflammation and fibrogenesis. Peroxisome proliferator-activated receptor (PPAR)-gamma is a receptor transcription factor that controls growth and differentiation in different tissues. We explored the effects of PPAR-gamma agonists on the biological actions of cultured human HSCs. HSCs were isolated from normal human liver tissue and used in their myofibroblast-like phenotype or immediately after isolation. Activation of PPAR-gamma was induced with 15-deoxy-Delta(12, 14)-prostaglandin J(2) or with troglitazone. PPAR-gamma agonists dose-dependently inhibited HSC proliferation and chemotaxis induced by platelet-derived growth factor. This effect was independent of changes in postreceptor signaling or expression of c-fos and c-myc and was associated with inhibition of cell cycle progression beyond the G(1) phase. Activation of PPAR-gamma also resulted in a complete inhibition of the expression of monocyte chemotactic protein 1 at the gene and protein levels. Comparison of quiescent and culture-activated HSCs revealed a marked decrease in PPAR-gamma expression in activated cells.
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Activation of PPAR-gamma modulates profibrogenic and proinflammatory actions in HSCs. Reduced PPAR-gamma expression may contribute to confer an activated phenotype to HSCs. Final Decision: yes