title: miR-33a levels in hepatic and serum after chronic HBV-induced fibrosis.
abstract: BACKGROUND
  Chronic hepatitis B virus (HBV) infection, which can lead to hepatic disease, has become a critical national healthcare problem, and many people die each year as a result of HBV infection and its complications. Although microRNA-33a (miR-33a) is a novel modulator of lipid and cholesterol metabolism, the role of miR-33a in the hepatic fibrogenesis is still unknown. Here, we aimed to explore the roles and mechanisms of miR-33a in liver fibrosis.
  
  
  METHODS
  miR-33a expression in whole liver and serum samples was measured from chronic hepatitis B (CHB) patients by quantitative real-time PCR (qRT-PCR). In addition, different murine hepatic fibrosis models were produced to consolidate the results in human tissue. Human and murine primary liver fibrosis-associated cells were isolated and treated with transforming growth factor-β1 (TGF-β1).
  
  
  RESULTS
  miR-33a expression levels in liver tissue significantly increased with a fibrosis progression manner in the human liver. Furthermore, serum miR-33a levels associated positively with progressing process of hepatic fibrosis. miR-33a was in particular increased in hepatic stellate cells (HSC) than other liver fibrosis-associated cells. Stimulation of HSCs with TGF-β1 leads to a critical increase of miR-33a. Increasing miR-33a levels increased (whereas inhibiting miR-33a weakened) the activation role of TGF-β1 in LX-2 cells, which might be a potential mechanism through moderating Smad7 expression.
  
  
  CONCLUSIONS
  miR-33a may be a novel marker for HSC activation and hepatic fibrosis progress, suggesting a new therapeutic target in liver fibrosis.
authors.affiliation: Department of Occupational and Environmental Health, School of Public Health, Wuhan University, Wuhan, 430071, China.
authors.forename: Chuan-Feng
authors.initials: CF
authors.lastname: Huang
authors.forename: Cheng-Chao
authors.initials: CC
authors.lastname: Sun
authors.forename: Fang
authors.initials: F
authors.lastname: Zhao
authors.forename: Ya-Dong
authors.initials: YD
authors.lastname: Zhang
authors.forename: De-Jia
authors.initials: DJ
authors.lastname: Li
mesh_terms: D000328:Adult; D000818:Animals; D002478:Cells, Cultured; D018450:Disease Progression; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D055166:Hepatic Stellate Cells / Q000378:metabolism; D019694:Hepatitis B, Chronic / Q000150:complications*; D022781:Hepatocytes / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D008099:Liver / Q000378:metabolism*; D008103:Liver Cirrhosis / Q000235:genetics* / Q000821:virology; D008297:Male; D008810:Mice, Inbred C57BL; D035683:MicroRNAs / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D008875:Middle Aged; D012333:RNA, Messenger / Q000235:genetics; D012720:Severity of Illness Index; D051906:Smad7 Protein / Q000235:genetics / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000494:pharmacology / Q000502:physiology
chemical_list: C550416:MIRN33a microRNA, human; D035683:MicroRNAs; D012333:RNA, Messenger; C497806:SMAD7 protein, human; D051906:Smad7 Protein; D053773:Transforming Growth Factor beta1