Diesel exhaust particles inhibit lung branching morphogenesis via the YAP/TAZ pathway
Science of The Total Environment, ISSN: 0048-9697, Vol: 861, Page: 160682
2023
- 3Citations
- 10Captures
- 1Mentions
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- Citations3
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Taipei Medical University Reports Findings in Ecology, Environment and Conservation (Diesel exhaust particles inhibit lung branching morphogenesis via the YAP/TAZ pathway)
2022 DEC 16 (NewsRx) -- By a News Reporter-Staff News Editor at Taiwan Daily Report -- New research on Ecology, Environment and Conservation is the
Article Description
Prenatal exposure to air pollution may associated with inhibition of lung development in the child, however the possible mechanism is unclear. We investigated the effects of traffic-related diesel exhaust particle (DEP) exposure on fetal lung branching morphogenesis and elucidate the possible mechanism. Ex vivo fetal lungs collected from ICR mice at an age of 11.5 embryonic (E) days were exposed to DEPs at 0 (control), 10, and 50 μg/mL and branching morphogenesis was measured for 3 days. Normal IMR-90 human fetal lung fibroblast cells were exposed to DEPs at 0 (control), 10, and 50 μg/mL for 24 h. We observed that DEP exposure significantly inhibited lung branching morphogenesis with reduced lung branching ratios and surface areas on day 3. RNA sequencing (RNA-Seq) showed that DEP increased the inflammatory response and impaired lung development-related gene expressions. DEPs significantly decreased Yes-associated protein (YAP), phosphorylated (p)-YAP, transcriptional coactivator with a PDZ-binding motif (TAZ), and p-TAZ in IMR-90 cells at 10 and 50 μg/mL. Treatment of fetal lungs with the YAP inhibitor, PFI-2, also demonstrated restricted lung branching development similar to that of DEP exposure, with a significantly decreased lung branching ratio on day 3. DEP exposure significantly decreased the lung branching modulators fibroblast growth factor receptor 2 (FGFR2), sex-determining region Y-box 2 (SOX2), and SOX9 in IMR-90 cells at 10 and 50 μg/mL. Fetal lung immunofluorescence staining showed that DEP decreased SOX2 expression in fibronectin + fibroblasts. DEP exposure decreased the cellular senescence regulator, p-sirtuin 1 (SIRT1)/SIRT1 in IMR-90 cells, with RNA-Seq showing impaired telomere maintenance. DEP exposure impaired fetal lung growth during the pseudoglandular stage through dysregulating the Hippo signaling pathway, causing fibroblast lung branching restriction and early senescence. Prenatal exposure to traffic-related air pollution has adverse effects on fetal lung development.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0048969722077853; http://dx.doi.org/10.1016/j.scitotenv.2022.160682; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85145552994&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/36481141; https://linkinghub.elsevier.com/retrieve/pii/S0048969722077853; https://dx.doi.org/10.1016/j.scitotenv.2022.160682
Elsevier BV
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