title: Pathogenesis pathways of idiopathic pulmonary fibrosis in bleomycin-induced lung injury model in mice.
abstract: Our objective was to investigate the pathogenesis pathways of idiopathic pulmonary fibrosis (IPF). Bleomycin (BLM) induced animal models of experimental lung fibrosis were used. CHIP assay was executed to find the link between Smad3 and IL-31, and the expressions of TGF-β1, Smad3, IL-31 and STAT1 were detected to find whether they were similar with each other. We found that in the early injury or inflammation of the animal model, BLM promoted the development of inflammation, leading to severe pulmonary fibrosis. Then the expression of TGF-β1 and Smad3 increased. Activated Smad3 bound to the IL-31 promoter region, followed by the activation of JAK-STAT pathways. The inhibitor of TGF-β1 receptor decreased the IL-31 expression and knocking-down of IL-31 also decreased the STAT1 expression. We conclude that there is a pathway of pathogenesis in BLM-induced mouse model that involves the TGF-β, IL-31 and JAKs/STATs pathway.
authors.affiliation: Department of Geriatrics, The Affiliated Yixing Hospital of Jiangsu University, Yixing, Jiangsu, China. Electronic address: shikeyun@foxmail.com.
authors.forename: Keyun
authors.initials: K
authors.lastname: Shi
authors.forename: Jianzhong
authors.initials: J
authors.lastname: Jiang
authors.forename: Tieliang
authors.initials: T
authors.lastname: Ma
authors.forename: Jing
authors.initials: J
authors.lastname: Xie
authors.forename: Lirong
authors.initials: L
authors.lastname: Duan
authors.forename: Ruhua
authors.initials: R
authors.lastname: Chen
authors.forename: Ping
authors.initials: P
authors.lastname: Song
authors.forename: Zhixin
authors.initials: Z
authors.lastname: Yu
authors.forename: Chao
authors.initials: C
authors.lastname: Liu
authors.forename: Qin
authors.initials: Q
authors.lastname: Zhu
authors.forename: Jinxu
authors.initials: J
authors.lastname: Zheng
mesh_terms: D000818:Animals; D000903:Antibiotics, Antineoplastic / Q000633:toxicity*; D001549:Benzamides / Q000494:pharmacology; D001761:Bleomycin / Q000633:toxicity*; D002478:Cells, Cultured; D004149:Dioxoles / Q000494:pharmacology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects*; D054990:Idiopathic Pulmonary Fibrosis / Q000209:etiology* / Q000378:metabolism*; D007378:Interleukins / Q000235:genetics / Q000378:metabolism; D008168:Lung / Q000166:cytology; D055370:Lung Injury / Q000139:chemically induced* / Q000150:complications*; D051379:Mice; D050794:STAT1 Transcription Factor / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects* / Q000502:physiology; D013997:Time Factors; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism
chemical_list: C459179:4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide; D000903:Antibiotics, Antineoplastic; D001549:Benzamides; D004149:Dioxoles; D004791:Enzyme Inhibitors; D007378:Interleukins; D050794:STAT1 Transcription Factor; C494080:Stat1 protein, mouse; D053773:Transforming Growth Factor beta1; C502588:interleukin-31, mouse; D001761:Bleomycin
keywords: Bleomycin; IL-31; Idiopathic pulmonary fibrosis; JAK-STAT; Lung; Smad3