You, Jie; Wu, Wenyu; Lu, Mengxin; Xie, Yanghao; Miao, Rui; Gu, Misi; Xi, Dong; Yan, Weiming; Wu, Di; Wang, Xiaojing; Chen, Tao; Ning, Qin; Han, Meifang published the artcile< Hepatic exosomes with declined MiR -27b-3p trigger RIG-I / TBK1 signal pathway in macrophages>, Synthetic Route of 6823-69-4, the main research area is miR27b3p RIGI TBK1 macrophage hepatic exosome signaling pathway; HBsAg; exosome; host immune; interferon alpha; miR-27b-3p.
Evidence suggests that interferon alpha (IFNα) plays an essential role in decreasing the HBsAg quantification and elevating the rate of clin. cure in chronic hepatitis B (CHB). However, the mechanisms underlying the effects of the exosomes on the expression of host genes in IFNα treatment remain unclear. CHB patients with IFNα treatment were divided into responders and non-responders according to the degree of HBsAg decline. Through microRNA sequencing and a series of mol. biol. methods, the key microRNAs in serum exosomes associated with clin. antiviral response of Peg-IFNα treatment in nucleotide analog-treated CHB patients were investigated. The roles of exosomal miRNAs on the IFNα signal pathway were explored in macrophages. MicroRNA sequencing and RT-qPCR assays confirmed six distinctly declined miRNAs in serum exosomes of responders at week 12 compared with levels at baseline. Exosomes with declined miR27b-3p in the serum of Peg-IFNα-treated responders activated phosphorylation of interferon regulatory factor 3/7 (IRF3/7) in IFNα synthesis pathway in macrophages. However, miR-27b-3p overexpression in HepAD38 cells suppressed IFNα synthesis in macrophages, resulting in insufficient ability to eliminate HBV, whereas the inhibitory effect could be blocked by inhibitors of exosomes release. Luciferase assay showed miR-27b-3p directly suppressed retinoic acid-inducible gene I (RIG-I) and TANK-binding kinase 1 (TBK1) expressions, and these effects could be abrogated in mutation experiments In IFNα treatment, exosomes with declined miR-27b-3p triggered activation of RIG-I/TBK1 signalling in macrophages against HBV. Serum exosomal miR-27-3p might represent a potential biomarker for patients with CHB.
Liver International published new progress about Antiviral agents. 6823-69-4 belongs to class imidazoles-derivatives, and the molecular formula is C30H30Cl2N6O2, Synthetic Route of 6823-69-4.
Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem