cyanoginosin-lr and Idiopathic-Pulmonary-Fibrosis

Idiopathic pulmonary fibrosis (IPF) is a group of chronic interstitial pulmonary diseases characterized by myofibroblast proliferation and extracellular matrix deposition with limited treatment options. Based on our previous observation, we hypothesized microcystin-leucine arginine (LR), an environmental cyanobacterial toxin, could potentially suppress pulmonary fibrosis. In this study, we first demonstrated that chronic exposure of microcystin-LR by oral for weeks indeed attenuated the pulmonary fibrosis both on bleomycin-induced rat and fluorescein isothiocyanate-induced mouse models. Our data further indicated that treatment with microcystin-LR substantially reduced TGF-β1/Smad signaling in rat pulmonary tissues. The experiments in vitro found that microcystin-LR was capable of blocking epithelial-mesenchymal transition (EMT) and fibroblast-myofibroblast transition (FMT) through suppressing the differentiation of CD206

Topics: A549 Cells; Animals; Disease Models, Animal; Endoplasmic Reticulum Chaperone BiP; Fibroblasts; Heat-Shock Proteins; Humans; Idiopathic Pulmonary Fibrosis; Lectins, C-Type; Lung; Macrophages; Male; Mannose Receptor; Mannose-Binding Lectins; Marine Toxins; Mice; Mice, Inbred C57BL; Microcystins; NIH 3T3 Cells; Phenotype; Protein Phosphatase 2; Rats, Sprague-Dawley; RAW 264.7 Cells; Receptors, Cell Surface; Signal Transduction; Smad Proteins; Transforming Growth Factor beta1