In several organs, the lineages of stem cells, fate committed progenitor cells, and terminal differentiated cells are well documented. Progenitor/stem cells are cells with a capacity for self-renewal and differentiation to regenerate adult tissues. The immunologic interaction between hepatic parenchyma cells and encircling inflammatory cells is thought to be the most important mechanism underlying biliary damage and repair. Convincing human leukocyte antigen (HLA) gene correlations, in association with gene signatures representing T-cell function, supports the implication of acquired immunity in PSC pathogenesis and categorizes PSC as an autoimmune disease. Though the etiology and pathogenic mechanisms currently warrant further elucidation, the gene expression profiles of PSC are regarded as sharing traits with both inflammatory bowel disease and autoimmune diseases. Dynamic cholangiocyte damage eventually results in cholangiocyte death, regeneration, and fibrosis-cirrhosis. Primary sclerosing cholangitis (PSC) is a life-long liver disease characterized by chronic cholangitis associated with destruction of intra- and extrahepatic bile ducts. In the liver of PSC patients, the prevalence of activated macrophages, with M1 polarized accounting for the main part, is associated with increment of Notch signalling and enhancement of HPC self-renewal. These findings suggest that M1 macrophages promote an HPC self-renewing phenotype which is associated with Notch signalling activation within HPC. GSEA data show that macrophage activation and Notch signalling-associated gene signatures are enriched in PSC patients. Blocking Jagged1 by siRNA or antibody in the coculture system attenuates HPC self-renewing phenotypes as well as HES1 expression in HPC. M1 macrophages were found associated with elevated Jag1 expression, which increased the fraction of HPC with self-renewing phenotypes (CD326 +CD44 + or CD324 +CD44 +) and HES1 expression level in cocultured HPC. Monocyte-macrophage and Notch signalling-associated gene signatures were evaluated in the GEO database (access ID: GSE61260) by gene set enrichment analysis (GSEA). The effects of polarized BMDMs on the expression of hepatic progenitor cell- (HPC-) specific markers and hairy and enhancer of split-1 (HES1) in HPCs in coculture were also analyzed. Then, the expression levels of Jagged1 ( Jag1) of each phenotype were measured.
M1 or M2 macrophages were generated from mouse bone marrow-derived macrophages (BMDMs) by classical or alternative activation, respectively. We analyzed the expression of Notch ligand Jagged1 in polarized macrophages and investigated the relevance of Notch signalling activation in liver regeneration.
Macrophages coordinate with liver regeneration, and multiple phenotypes have been identified with diverse expressions of surface proteins and cytokine productions. Monocytes/macrophages as master regulators of hepatic inflammation have been demonstrated to contribute to PSC pathogenesis.
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Code Ann § 23-15-17.The immunologic interaction between parenchyma cells and encircling inflammatory cells is thought to be the most important mechanism of biliary damage and repair in primary sclerosing cholangitis (PSC).
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