Role of SCGB3A2 in pulmonary fibrosis

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An explosive number of people are affected by fibrosis worldwide in these days, and the morbidity and mortality rates are increasing every year. The exploration and/or development of a definitive medicine are urgently required. We report that SCGB3A2 drastically reduces the severity of lung fibrosis using bleomycin (BLM)-induced mouse model. Mice were intravenously administered SCGB3A2 for 7 days starting at day 14 after administration of BLM by intratracheal intubation. Fibrosis foci were remarkably reduced by SCGB3A2 in lung lobes and the number of neutrophils and macrophages was also reduced in branchoalveolar lavage fluid (BALF). Additionally, when lung fibroblast cells isolated from adult mice were differentiated into myofibroblast cells by TGFβ, the differentiation was inhibited by SCGB3A2 as judged by morphology and reduced expression of a smooth muscle actin (αSMA). Collagen 1a2 and 3a1 gene expression was also decreased in the presence of SCGB3A2.