2026-10-11T08:08:59Z https://api.figshare.com/v2/oai

oai:figshare.com:article/33718342 2026-09-14T04:37:48Z category_696 portal_316 item_type_3 month_year_09_2026

Table 2_Adipose-derived mesenchymal stem cell-exosomes attenuate lipopolysaccharide-induced acute lung injury in mice by regulating the TGFBR2/Smad4 axis to suppress NLRP3-mediated macrophage M1 polarization and pyroptosis.docx Jie Li (15030) Huan Kang (5755496) Baolong Wang (6329198) Fangqiang Zou (24867754) Wei Liu (20030) Weixin Guo (24867757) Xinliang Liao (24867760) Genetic Immunology adipose-derived mesenchymal stem cells exosomes LPS-induced acute lung injury lung epithelial cells macrophages microRNA-19b-3p pyroptosis transforming growth factor beta receptor II Objective<p>This study investigated whether adipose-derived mesenchymal stem cells-exosomes (ADMSC-Exo) alleviate lipopolysaccharide (LPS)-induced acute lung injury (ALI) by regulating NLRP3 inflammasome-mediated macrophage M1 polarization and pyroptosis through the miR-19b-3p/TGFBR2/Smad4 signaling axis.</p>Methods<p>An LPS-induced mouse model of ALI was established and treated with ADMSC-Exo or adenoviral TGFBR2 overexpression (Ad-TGFBR2). Lung histopathology, lung wet-to-dry (W/D) weight ratio, macrophage polarization, and pyroptosis were evaluated. In vitro, macrophages with TGFBR2 knockdown or overexpression were stimulated with LPS and treated with ADMSC-Exo. Lung epithelial cells were subsequently cultured with macrophage-conditioned medium. The expression of miR-19b-3p, TGFBR2, mothers against decapentaplegic homolog 4 (Smad4), and NOD-like receptor protein 3 (NLRP3), together with macrophage polarization, pyroptosis, and epithelial cell apoptosis, was assessed. Predicted molecular interactions were validated using bioinformatic analyses and the JASPAR database.</p>Results<p>ADMSC-Exo alleviated LPS-induced lung injury by preserving alveolar architecture and reducing lung injury scores and the W/D ratio. They inhibited M1 macrophage polarization and pyroptosis both in vivo and in vitro, thereby decreasing apoptosis of lung epithelial cells. Mechanistically, ADMSC-Exo-delivered miR-19b-3p, which targeted TGFBR2 and inhibited TGFBR2/Smad4 signaling, resulting in transcriptional suppression of NLRP3 expression. Inhibition of miR-19b-3p or overexpression of Smad4/NLRP3 partially abolished the protective effects of ADMSC-Exo. Collectively, ADMSC-Exo attenuated LPS-induced ALI by suppressing NLRP3-mediated macrophage M1 polarization and pyroptosis through the miR-19b-3p/TGFBR2/Smad4 signaling axis.</p>Conclusion<p>ADMSC-derived exosomes alleviate LPS-induced acute lung injury by delivering miR-19b-3p to inhibit the TGFBR2/Smad4 signaling pathway, thereby suppressing NLRP3-mediated macrophage M1 polarization and pyroptosis and reducing lung epithelial cell apoptosis.</p> 2026-09-14T04:37:48Z Dataset Dataset 10.3389/fimmu.2026.1739115.s005 https://figshare.com/articles/dataset/Table_2_Adipose-derived_mesenchymal_stem_cell-exosomes_attenuate_lipopolysaccharide-induced_acute_lung_injury_in_mice_by_regulating_the_TGFBR2_Smad4_axis_to_suppress_NLRP3-mediated_macrophage_M1_polarization_and_pyroptosis_docx/33718342 CC BY 4.0