title: Studying the association of microRNA-210 level with chronic hepatitis B progression.
abstract: We studied the relationship between hypoxia and microRNA-210 (miR-210) levels, the miR-210 levels in patients with hepatitis B and the roles of miR-210 in liver inflammation. We used the concanavalin A (Con A) murine hepatitis model and inflammation, hypoxia and miR-210 levels were examined. In these patients, we studied serum miR-210 levels and clinical indexes related to hepatitis in 90 patients with different stages of chronic hepatitis B and 30 controls. Two functional assays of miR-210 in vitro under hypoxic condition were conducted. The animal experiments indicated that the liver and serum miR-210 levels significantly increased with liver hypoxia and inflammation. In humans, serum miR-210 levels enhanced with hepatitis severity and were related to serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TB) and prothrombin activity (PTA) levels. The miR-210 functional assays showed that miR-210 elevation might be related to the decreases in HepG2.2.15 cell dehydrogenase activity and HBV replication under hypoxic conditions. Because the liver inflammation causes liver hypoxia which also results in liver and serum miR-210 level elevation, the serum miR-210 level may serve as a molecular biomarker for the severity of hepatitis and increases in liver miR-210 that we see may be a response of hepatocytes to hypoxia during hepatitis progression.
authors.affiliation: State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China; Department of Etiology, Zhejiang Academy of Medical Sciences, Hangzhou, Zhejiang, China.
authors.forename: G
authors.initials: G
authors.lastname: Song
authors.forename: H
authors.initials: H
authors.lastname: Jia
authors.forename: H
authors.initials: H
authors.lastname: Xu
authors.forename: W
authors.initials: W
authors.lastname: Liu
authors.forename: H
authors.initials: H
authors.lastname: Zhu
authors.forename: S
authors.initials: S
authors.lastname: Li
authors.forename: J
authors.initials: J
authors.lastname: Shi
authors.forename: Z
authors.initials: Z
authors.lastname: Li
authors.forename: J
authors.initials: J
authors.lastname: He
authors.forename: Z
authors.initials: Z
authors.lastname: Chen
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D001663:Bilirubin / Q000097:blood; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D045744:Cell Line, Tumor; D056486:Chemical and Drug Induced Liver Injury / Q000097:blood / Q000503:physiopathology; D003208:Concanavalin A / Q000009:adverse effects; D004195:Disease Models, Animal; D018450:Disease Progression; D005260:Female; D006515:Hepatitis B virus / Q000235:genetics* / Q000502:physiology; D019694:Hepatitis B, Chronic / Q000097:blood* / Q000235:genetics / Q000503:physiopathology; D006801:Humans; D000860:Hypoxia / Q000139:chemically induced / Q000503:physiopathology*; D008099:Liver / Q000503:physiopathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D035683:MicroRNAs / Q000097:blood* / Q000235:genetics / Q000378:metabolism; D008875:Middle Aged; D011516:Prothrombin / Q000378:metabolism; D013047:Specific Pathogen-Free Organisms; D014779:Virus Replication
chemical_list: D015415:Biomarkers; C543800:MIRN210 microRNA, human; D035683:MicroRNAs; D003208:Concanavalin A; D011516:Prothrombin; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D001663:Bilirubin
keywords: biomarker; chronic hepatitis B; hepatitis progression; hypoxia; inflammation; miR-210