Circulating MicroRNAs in Plasma of Hepatitis B e Antigen Positive Children Reveal Liver-Specific Target Genes. (17th December 2014)

• Record Type: Journal Article
• Authors: Winther, Thilde Nordmann; Jacobsen, Kari Stougaard; Mirza, Aashiq Hussain; Heiberg, Ida Louise; Bang-Berthelsen, Claus Heiner; Pociot, Flemming; Hogh, Birthe
• Other Names: Morioka Daisuke Academic Editor.
• Is Part Of: International journal of hepatology. Volume 2014(2014)
• Publication Date: 2014-12-17
• Subjects: Hepatology -- Periodicals; Liver Diseases; Gastroenterology; Hepatology; Electronic journals; Periodicals; Periodicals; Fulltext; Internet Resources; Periodicals; 616.3
• DOI: 10.1155/2014/791045
• Languages: English
• ISSNs: 2090-3448

Abstract

Abstract : Background and Aim . Hepatitis B e antigen positive (HBeAg-positive) children are at high risk of severe complications such as hepatocellular carcinoma and cirrhosis. Liver damage is caused by the host immune response to infected hepatocytes, and we hypothesise that specific microRNAs play a role in this complex interaction between virus and host. The study aimed to identify microRNAs with aberrant plasma expressions in HBeAg-positive children and with liver-specific target genes. Methods . By revisiting our previous screen of microRNA plasma levels in HBeAg-positive and HBeAg-negative children with chronic hepatitis B (CHB) and in healthy controls, candidate microRNAs with aberrant plasma expressions in HBeAg-positive children were identified. MicroRNAs targeting liver-specific genes were selected based on bioinformatics analysis and validated by qRT-PCR using plasma samples from 34 HBeAg-positive, 26 HBeAg-negative, and 60 healthy control children. Results . Thirteen microRNAs showed aberrant plasma expressions in HBeAg-positive children and targeted liver-specific genes. In particular, three microRNAs were upregulated and one was downregulated in HBeAg-positive children compared to HBeAg-negative and healthy control children, which showed equal levels. Conclusion . The identified microRNAs might impact the progression of CHB in children. Functional studies are warranted, however, to elucidate the microRNAs' role in the immunopathogenesis of childhood CHB.