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Your search keyword '"Ji, Junsong"' showing total 2 results
Start Over Author "Ji, Junsong" Topic influenza, human
2 results on '"Ji, Junsong"'

1. Inhibition of miR-93 promotes interferon effector signaling to suppress influenza A infection by upregulating JAK1.

Author

Guo M, Li F, Ji J, Liu Y, Liu F, Zhao Y, Li J, Han S, Wang Q, and Ding G

Subjects
Animals, Antagomirs administration & dosage, Cell Line, Gene Expression Regulation, Humans, Interferons genetics, Interferons metabolism, Janus Kinase 1 genetics, Janus Kinase 1 metabolism, MAP Kinase Kinase 4 metabolism, Male, Mice, Mice, Inbred C57BL, Receptors, Cell Surface metabolism, Signal Transduction, Influenza A virus physiology, Influenza, Human immunology, MicroRNAs genetics, Orthomyxoviridae Infections immunology
Abstract

Type I interferons play a critical role in host defense against influenza virus infection. Interferon cascade induces the expression of interferon-stimulated genes then subsequently promotes antiviral immune responses. The microRNAs are important regulators of innate immunity, but microRNAs-mediated regulation of interferon cascade during influenza infection remains to be fully identified. Here we found influenza A virus (IAV) infection significantly inhibited miR-93 expression in alveolar epithelial type II cells through RIG-I/JNK pathway. IAV-induced downregulation of miR-93 was found to upregulate JAK1, the target of miR-93, and then feedback promote antiviral innate response by facilitating IFN effector signaling. Importantly, in vivo administration of miR-93 antagomiR markedly suppressed IAV infection, protecting mice form IAVs -associated death. Hence, the inducible downregulation of miR-93 feedback suppress IAV infection by strengthening IFN-JAK-STAT pathway via JAK1 upregulation, and in vivo inhibition of miR-93 bears considerable therapeutic potential for suppressing IAV infection., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Published
2020
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2. Inhibition of miR-93 promotes interferon effector signaling to suppress influenza A infection by upregulating JAK1

Author

Yuanyu Zhao, Li Fangbing, Junhui Li, Ji Junsong, Fang Liu, Quanxing Wang, Guoshan Ding, Liu Yanfang, Shu Han, and Guo Meng

Subjects
Male, 0301 basic medicine, MAP Kinase Kinase 4, Immunology, Receptors, Cell Surface, Biology, medicine.disease_cause, Virus, Cell Line, Mice, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Immune system, Orthomyxoviridae Infections, Downregulation and upregulation, Interferon, Influenza, Human, Influenza A virus, medicine, Animals, Humans, Immunology and Allergy, Antagomir, Pharmacology, Innate immune system, Effector, Antagomirs, Janus Kinase 1, Mice, Inbred C57BL, MicroRNAs, 030104 developmental biology, Gene Expression Regulation, chemistry, 030220 oncology & carcinogenesis, Cancer research, Interferons, Signal Transduction, medicine.drug
Abstract

Type I interferons play a critical role in host defense against influenza virus infection. Interferon cascade induces the expression of interferon-stimulated genes then subsequently promotes antiviral immune responses. The microRNAs are important regulators of innate immunity, but microRNAs-mediated regulation of interferon cascade during influenza infection remains to be fully identified. Here we found influenza A virus (IAV) infection significantly inhibited miR-93 expression in alveolar epithelial type II cells through RIG-I/JNK pathway. IAV-induced downregulation of miR-93 was found to upregulate JAK1, the target of miR-93, and then feedback promote antiviral innate response by facilitating IFN effector signaling. Importantly, in vivo administration of miR-93 antagomiR markedly suppressed IAV infection, protecting mice form IAVs -associated death. Hence, the inducible downregulation of miR-93 feedback suppress IAV infection by strengthening IFN-JAK-STAT pathway via JAK1 upregulation, and in vivo inhibition of miR-93 bears considerable therapeutic potential for suppressing IAV infection.

Published
2020

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