8‐Oxoguanine DNA glycosylase modulates the cell transformation process in pulmonary fibrosis by inhibiting Smad2/3 and interacting with Smad7

• DOI: 10.1096/fj.201901291rrrrr
• Publication Date: 2020-08-28T04:55:27Z
• Authors: Yahong Wang; Ting Chen; Zhanchun Pan; Ziying Lin; Lawei Yang; Baoan Zou; Weimin Yao; Dehui Feng; Changmei Huangfu; Chunyu Lin; Guiqing Wu; Huayu Ling; Gang Liu
• Keywords: Mice, Knockout; 0301 basic medicine; 0303 health sciences; Pulmonary Fibrosis; Smad2 Protein; Fibroblasts; DNA Glycosylases; Rats; Smad7 Protein; Mice, Inbred C57BL; Transforming Growth Factor beta1; Mice; 03 medical and health sciences; A549 Cells; Alveolar Epithelial Cells; Animals; Humans; Smad3 Protein

The DNA repair enzyme 8-oxoguanine glycosylase-1 (OGG1) is involved in early embryonic development, as well multiple conditions, including cardiac fibrosis, diabetes, and neurodegenerative diseases. But, function of OGG1 pulmonary fibrosis was not entirely clear. In this study, we identified a novel the cell transformation process fibrosis. We demonstrated that Smad7 co-localize interact A549 cells. Bleomycin-induced established wild-type (WT) Ogg1-/- mice. Upon treatment with transforming growth factor (TGF)-β1, increased expression observed WT mice cells, MRC-5 primary rat type II alveolar epithelial promoted migration, while depletion decreased migration ability. Expression transformation-associated markers vimentin alpha-smooth muscle actin were also affected by OGG1. TGF-β1-induced activated Smad2/3 interacting Smad7. interaction between TGF-β/Smad axis modulates lung cells fibroblasts. Moreover, Ogg1 deficiency relieved bleomycin-treated knockout bleomycin-induced phosphorylation These findings suggest has biological functions pathogenesis