Hepatitis B virus confers innate immunity evasion through hepatitis B virus-miR-3 down-regulation of cGAS-Sting-IFN signaling.

Background: Hepatitis B virus (HBV) evades the innate immunity and leads to persistent chronic infection, but the molecular mechanism is still not well known.

Aim: To investigate whether HBV-miR-3 is involved in HBV immune evasion.

Methods: HBV-miR-3 agomir and antagomir were employed to verify the effectiveness of HBV-miR-3 on cGAS-Sting-IFN pathway through the experiments on relative luciferase activity, cGAS protein expression, Sting phosphorylation and interferon (IFN) production.

OPN-Mediated Crosstalk Between Hepatocyte E4BP4 and Hepatic Stellate Cells Promotes MASH-Associated Liver Fibrosis.

Stressed hepatocytes promote liver fibrosis through communications with hepatic stellate cells (HSCs) during chronic liver injury. However, intra-hepatocyte players that facilitate such cell-to-cell communications are largely undefined. It is previously reported that hepatocyte E4BP4 is potently induced by ER stress and hepatocyte deletion of E4bp4 protects mice from high-fat diet-induced liver steatosis.

Effects of climate and environment on migratory old people with allergic diseases in China: Protocol for a Sanya cohort study.

Background: Several studies have reported that the mountain climate can alleviate asthma, however, the effect of tropical climate on migratory elderly, especially in people with respiratory or allergic diseases is unknown.

Objectives: This cohort study aims to explore impact of climate and environmental changes on allergic diseases in migratory old people.

Methods: In this prospective cohort study, we recruited 750 older migratory people, the majority of whom were homeowners to minimize the risk of loss to follow up.

Igf2bp2 knockdown improves CCl-induced liver fibrosis and TGF-β-activated mouse hepatic stellate cells by regulating Tgfbr1.

Progressive liver fibrosis is a dynamic process characterized by the net accumulation of extracellular matrix (ECM), which could eventually develop into cirrhosis, leading to malignant transformation. In this study, insulin-like growth factor 2 mRNA binding protein 2 (Igf2bp2) was found to be up-regulated in carbon tetrachloride (CCl)-induced liver fibrosis and transforming growth factor-beta 1 (TGF-β)-activated hepatic stellate cells (HSCs). Igf2bp2 knockdown in the CCl-induced hepatic fibrosis mice model significantly improved CCl-induced liver damage by decreasing necrosis and fibrotic septa, reducing hydroxyproline levels, and down-regulating fibrotic markers levels.