Macrophage migration inhibitory factor promotes lung fibrosis via reactive oxygen species-mediated up-regulation of aerobic glycolysis

• Published in: Nan fang yi ke da xue xue bao = Journal of Southern Medical University Vol. 38; no. 7; p. 873
• Main Authors: Gao, Yun, Chen, Yu, Yu, Huaping, Lan, Haibing
• Format: Journal Article
• Language: Chinese
• Published: China 30.07.2018
• Subjects: macrophage migration inhibitory factor; aerobic glycolysis; lung fibrosis; reactive oxygen species
• ISSN: 1673-4254
• DOI: 10.3969/j.issn.1673-4254.2018.07.17

To explore the role of macrophage migration inhibitory factor (MIF) in lung fibrosis and the possible molecular pathways involved. Twenty male adult mice were randomized into control group and pulmonary fibrosis model group to receive intratracheal instillation of normal saline and bleomycin, respectively. Thirty days after the instillation, the level of MIF in the lung tissue of the mice was measured. Human embryonic lung fibroblasts (HLFs) were stimulated with recombinant human MIF (rMIF) and the changes in reactive oxygen species (ROS) levels, aerobic glycolysis and collagen production were measured; the effects of ROS inhibitor and glycolysis inhibitor on collagen productions were tested in rMIFstimulated HLF cells. Compared with the control mice, the mice with bleomycin-induced lung fibrosis exhibited significantly increased levels of MIF in the lung tissue and bronchoalveolar lavage fluid (BALF). ROS levels, aerobic glycolysis and collagen production were all increased in HLFs in response to rMIF stimul