ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
LncRNA SNHG14 drives alveolar inflammation in bronchopulmonary dysplasia via DNMT3a-mediated epigenetic silencing of miR-214-3p.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
OBJECTIVE AND
designThis experimental study investigated whether lncRNA SNHG14 contributes to hyperoxia-associated bronchopulmonary dysplasia (BPD) through DNMT3a-mediated epigenetic regulation of miR-214-3p and evaluated TfR-modified exosome-mimetic nanovesicles as an siRNA delivery platform. MATERIAL OR SUBJECTS: Hyperoxia-exposed murine alveolar epithelial type II cells and neonatal C57BL/6J mice were used. TREATMENT: Cells and neonatal mice were exposed to 85% O2 or normoxia. In vivo groups included normoxia, BPD, BPD + blank EMNVs, BPD + free siSNHG14, BPD + TfR-EMNVs-siSNHG14, and BPD + TfR-EMNVs-siSNHG14 + miR-214-3p antagomir.
methodsTranscriptomic, miRNA, methylation, pull-down, RIP, ChIP-qPCR, luciferase, biodistribution, histological, biochemical, and exploratory innate immune assays were performed.
resultsSNHG14 was upregulated after hyperoxia. SNHG14 silencing reduced epithelial injury, apoptosis, inflammation, and EMT-related changes, and was associated with decreased DNMT3a enrichment and methylation at the examined miR-214-3p promoter region. TfR-EMNVs-siSNHG14 improved siRNA delivery and lung-preferential fluorescence accumulation without overt short-term liver, kidney, or interferon-response toxicity.
conclusionsThe SNHG14/DNMT3a/miR-214-3p axis may contribute to experimental BPD-like alveolar injury, and TfR-EMNVs-siSNHG14 warrants further pharmacokinetic, safety, and clinical-sample validation.
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