Investigation into the effect of hepatitis B virus on apoliprotein A1 expression and its mechanism
Department of Clinical Laboratory, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P. R. China
Lipids in Health and Disease 2014, 13:130 doi:10.1186/1476-511X-13-130Published: 13 August 2014
Hepatitis B virus (HBV) infection poses a serious threat to human health, with China being one of the highly affected countries. However, the pathogenesis of chronic hepatitis B (CHB) is still unclear. Apolipoprotein A1 (ApoA1) which represents the major protein component of high-density lipoprotein is normally secreted by hepatocytes. When hepatocytes are infected with HBV may lead to the disruption of ApoA1 secretion. In this study, we investigated the effect of HBV on ApoA1 expression and preliminarily explored its molecular mechanism of regulation for revealing the pathogenesis of CHB.
The expression of mRNA and protein of ApoA1 in Human HepG2 hepatoblastoma cells and subline HepG2.2.15 cells were performed by reverse transcription-polymerase chain reaction (RT-PCR) and Western-blot. The serum ApoA1, by the immune turbidimetric test, and high-density lipoprotein cholesterol (HDL-C) in CHB patients and healthy controls, based on the enzymatic method, were measured with autobiochemical analyzer. The statistical difference was analyzed by SPSS 13.0. HBV infectious clone, pHBV1.3, and ApoA1 gene promoter were co-transfected into HepG2, and the luciferase activity was determined. The changes of ApoA1 mRNA and protein expression were detected by RT-PCR and Western-blot method, after HepG2 cells were transfected with pHBV1.3.
The expression of ApoA1 mRNA and protein in HepG2.2.15 were lower than those in HepG2, and when compared with healthy controls, serum levels of ApoA1 and HDL-C in CHB patients were lower (P < 0.05). pHBV1.3 in HepG2 cells restrained the activity of ApoA1 promoter, mRNA and protein expression.
HBV could inhibit the expression of ApoA1 in vitro and in vivo.