Some intermediate hepatocytes at portal tract/parenchyma interfac

Some intermediate hepatocytes at portal tract/parenchyma interface were positive for MMP-2 and revealed intercellular junctions with HPCs. A closely spatial association between HPCs and singly vimentin-positive cells in DRs was recognized, although the cells with co-expression Everolimus of vimentin and NCAM were not identified. Cells with epithelial phenotype were negative for αSMA while some fibroblast-like cells expressing αSMA were present around DRs. CD4 and TGFβ positive Cells surrounding

DRs increased parallel with the severity of inflammation and fibrosis. Neither HPCs nor cells with EMT in the control group were found. Conclusion: HPCs occur from cholangiocytes in DRs and contribute to hepatic

fibrosis via EMT in hepatitis B virus-related liver diseases. To mesenchymal or to hepatocytic differentiation of HPCs depends on, at least in part, the adjustment of microenvironment TGFβ, presenting by infiltrating CD4+ T-cells responding to HBV infection. Key Word(s): 1. HBV; 2. progenitor cell; 3. EMT; 4. liver; Presenting Author: YONGWEI LI Additional Authors: MINGFEN ZHU, GANG LI Corresponding Author: YONGWEI LI Affiliations: the Third Affiliated Hospital of Sun Yat-sen University; the Sixth Hospital of Shanghai Jiao Tong University; the Third this website Affiliated Hospital of Sun Yat-sen University Objective: Hepatitis B virus (HBV) uses heparan sulfate proteoglycans (HSPG) for its initial attachment to hepatocytes[1], but little is known about proteoglycans in HBV infection. Methods: Full-length HBV genomes from four patients with chronic HBV infection were cloned as our prior methods [2]. HBV genomes were transfected to HepG2 cells with

Lipofectamine™ 2000. An integrative genomic analysis was performed in HepG2 cells respectively transfected with the four HBV genomes, HepG2.215 cells and HepG2 cells using Affymetrix Human Genome U133 Plus 2.0 Array (HG-U133_Plus_2). Differentially expressed genes were identified by relative quantitative PCR. Results: Of 47,000 transcripts and variants on the gene chip, serglycin was one of the most significantly altered genes. The levels of serglycin were significantly upregulated in the HepG2 cells 5-FU order transfected with HBV genomes, but downregulated in HepG2.215 cells. Conclusion: Different HBV infection status results in profound changes in global gene transcription patterns. Serglycin, a proteoglycan, implied a different expression pattern between transient and chronic HBV infection. The shedding of serglycin maybe for immune evasion or other mechanisms in HepG2.215 cells with chronic HBV infection. Further study about serglycin is needed to perform in HBV infection. Key Word(s): 1. Serglycin; 2. HepG2; 3. Proteoglycans; 4.

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