Abstract
It has been previously reported that hepatitisB e‑antigen (HBeAg) induces microRNA (miR)‑155 expression and promotes liver injury by increasing inflammatory cytokine production in macrophages. Moreover, it was previously demonstrated that miR‑210 alleviates lipopolysaccharide‑stimulated proinflammatory cytokine production in macrophages. In addition, accumulating evidence suggests that miR‑210 is able to suppress hepatitisB virus (HBV) replication in HepG2.2.15 cells. However, it remains unclear whether miR‑210, similar to miR‑155, affects the progress of hepatitisB by regulating macrophage function. Reverse transcription‑quantitative polymerase chain reaction analysis was used to detect miR‑210 levels in serum and cells. HBV‑associated antigens stimulated different types of macrophages and facilitated the observation of the effects of these antigens on miR‑210 expression in macrophages. Co‑culture of peripheral blood monocytes from healthy controls and the serum of patients with chronic hepatitisB (CHB) was conducted to evaluate the effect of HBV‑associated elements in the serum on the expression of the macrophage miR‑210 invivo. It was observed that miR‑210 expression levels were decreased in the peripheral blood monocytes (PBMs) and serum of patients with CHB and negatively associated with serum alanine aminotransferase and aspartate aminotransferase, but not other clinical parameters including hepatitisB surface antigen (HBsAg), HBeAg, anti‑HBe antibody (HBeAb) and hepatitisB core antibody (HBcAb) and HBV‑DNA. Notably, it was demonstrated that miR‑210 expression was not affected by treatment with HBV‑associated antigens in different types of macrophages. Notably, the serum of patients with CHB was able to markedly downregulate the miR‑210 expression of PBMs in healthy controls. These findings suggested that, unlike the induction of miR‑155 by HBeAg, there may be certain other elements, apart from HBV‑associated antigens, regulating miR‑210 levels in the serum and PBMs of patients with CHB that affect macrophage activation.
Highlights
MicroRNAs are endogenous, evolutionarily highly conserved, small noncoding RNAs, which are derived from the genomes of eukaryotic organisms and various viruses and have multiple functions in the regulation of gene expression in animals and plants [1,2]. miRNA‐210, a prototypical hypoxamir, is one of the most widely studied miRNAs [3,4]
To evaluate the effect of miR‐210 on hepatitis B virus (HBV) infection, peripheral blood monocytes (PBMs) and serum were collected from patients with chronic hepatitis B (CHB) or healthy controls and miR‐210 expression was assessed
There was no marked correlation between miR‐210 expression and hepatitis B surface antigen (HBsAg), hepatitis B e‐antigen (HBeAg), HBe antibody (HBeAb), hepatitis B core antibody (HBcAb) and HBV‐DNA in the serum (Figs. 1D‐H; 2D‐H)
Summary
MicroRNAs (miRNAs) are endogenous, evolutionarily highly conserved, small noncoding RNAs, which are derived from the genomes of eukaryotic organisms and various viruses and have multiple functions in the regulation of gene expression in animals and plants [1,2]. miRNA (miR)‐210, a prototypical hypoxamir, is one of the most widely studied miRNAs [3,4]. LI et al: HBV INHIBITS MACROPHAGE miR-210 EXPRESSION with systemic lupus erythematosus and rheumatoid arthritis compared with healthy controls [8]. These above data suggest that miR‐210 serves an indispensable role in the pathogenesis of numerous diseases. Being one of the most common inflammatory diseases in the world, hepatitis B virus (HBV) infection is the leading cause of hepatocellular carcinoma (HCC), in Asian countries [9,10,11]. The molecular mechanisms by which HBV infection leads to HCC are comparatively complex. Elucidating the mechanism of HBV infection is of particular importance
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