title: HBV promotes the proliferation of hepatic stellate cells via the PDGF-B/PDGFR-β             signaling pathway in vitro.
abstract: The activation of hepatic stellate cells (HSCs) is closely associated with             liver fibrosis in chronic hepatitis B virus (HBV) infection. However, the molecular             mechanisms leading to HSC activation remain unclear. It has been reported that             the platelet-derived growth factor-B (PDGF-B)/PDGF receptor-β (PDGFR-β) signaling             pathway is involved in this process. Thus, we investigated whether HBV and its             protein contribute to HSC proliferation by the PDGF-B/PDGFR-β signaling pathway.             HBV particles were purified from the supernatant of HepG2.2.15 cells by ultracentrifugation             and the cell lines carrying HBV preS, e, c or x genes were obtained. After incubation             with HBV particles or co-cultured with the cell lines expressed in the viral protein,             the proliferation of LX-2 cells, an HSC cell line, were detected by flow cyto-metry             and real-time PCR and the expression of molecules related to the PDGF-B/PDGFR-β             signaling pathway were further measured. Our results indicated that HBV particles,             c and x proteins promoted LX-2 proliferation and increased the mRNA levels of             PDGF-B, PDGFR-β, collagen-I and α-smooth muscle actin (α-SMA), as well as the             phosphorylation of PDGFR-β; however, the expression protein levels of PDGF-B and             PDGFR-β remained unchanged. In conclusion, HBV particles and HBV c and x proteins             promote HSC proliferation and fibrogenesis in vitro and the PDGF-B/PDGFR-β signaling             pathway is important in this process.
authors.affiliation: Liver Research Center, Beijing Friendship Hospital, Capital Medical                     University, Beijing, P.R. China.
authors.forename: Qixuan
authors.initials: Q
authors.lastname: Bai
authors.forename: Jing
authors.initials: J
authors.lastname: An
authors.forename: Xiaoning
authors.initials: X
authors.lastname: Wu
authors.forename: Hong
authors.initials: H
authors.lastname: You
authors.forename: Hong
authors.initials: H
authors.lastname: Ma
authors.forename: Tianhui
authors.initials: T
authors.lastname: Liu
authors.forename: Na
authors.initials: N
authors.lastname: Gao
authors.forename: Jidong
authors.initials: J
authors.lastname: Jia
mesh_terms: D000199:Actins / Q000235:genetics / Q000378:metabolism; D000077214:Becaplermin; D049109:Cell Proliferation; D018920:Coculture Techniques; D024042:Collagen Type I / Q000235:genetics / Q000378:metabolism; D056945:Hep G2 Cells; D055166:Hepatic Stellate Cells / Q000502:physiology* / Q000821:virology; D006515:Hepatitis B virus / Q000502:physiology*; D054884:Host-Pathogen Interactions; D006801:Humans; D008103:Liver Cirrhosis / Q000821:virology; D010766:Phosphorylation; D011499:Protein Processing, Post-Translational; D020574:Proto-Oncogene Proteins c-sis / Q000235:genetics / Q000378:metabolism*; D020797:Receptor, Platelet-Derived Growth Factor beta / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction; D015854:Up-Regulation; D014764:Viral Proteins / Q000502:physiology
chemical_list: D000199:Actins; D024042:Collagen Type I; D020574:Proto-Oncogene Proteins c-sis; D014764:Viral Proteins; D000077214:Becaplermin; D020797:Receptor, Platelet-Derived Growth Factor beta