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RNA-seq and ChIP-seq reveal microplastics induce endothelial-mesenchymal transition via HK2-mediated histone lactylation in pulmonary hypertension
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Using RNA-seq and ChIP-seq, researchers found that microplastics promote endothelial-to-mesenchymal transition in pulmonary artery cells through a pathway involving HK2-mediated histone lactylation, which contributes to pulmonary hypertension. This epigenetic mechanism provides a new molecular explanation for how microplastic exposure may drive vascular remodeling in the lungs.
Pulmonary hypertension (PH) is a life-threatening condition characterized by progressive pulmonary vascular remodeling, and endothelial-mesenchymal transition (EndMT) is recognized as a critical pathogenic process driving this remodeling. This study investigated the role of microplastics (MPs) in promoting EndMT in human pulmonary artery endothelial cells (HPAECs) and its underlying regulatory mechanism. We demonstrated that MPs were internalized by HPAECs, leading to significant downregulation of endothelial markers (CD31 and VE-cadherin) and upregulation of mesenchymal markers (α-SMA and vimentin), thereby promoting EndMT. In a rat model of PH induced by monocrotaline, intratracheal instillation of MPs further increased right ventricular and pulmonary arterial pressures, exacerbated vascular remodeling, and enhanced inflammatory infiltration. RNA-seq analysis revealed that MPs activated inflammatory pathways and enhanced glycolysis in HPAECs, with significant upregulation of glycolytic genes such as HK2. Knockdown of HK2 attenuated the cell viability and migratory ability of HPAECs and counteracted MP-induced EndMT. Additionally, MPs increased lactate production and histone lactylation, which were reversed by HK2 interference. ChIP-seq further confirmed the altered histone lactylation by MPs in HPAECs, including 603 genes with hyper-lactylation and 1292 genes with hypo-lactylation. Genes with hyper-lactylation were related to inflammation, and genes with hypo-lactylation were associated with epithelial/endothelial cell migration, angiogenesis, and vascular endothelial growth factor signaling pathway. Integrative analysis of the RNA-seq and ChIP-seq data identified four PH- and inflammation-associated differentially expressed genes exhibiting hyper-lactylation (FOXO3, RUNX1, TNFRSF11B, and SGK1). Among them, RT-PCR and ChIP-qPCR confirmed the upregulation and increased histone lactylation of TNFRSF11B and SGK1. These findings highlight the critical role of MPs in modulating metabolic and histone lactylation in PH and suggest potential therapeutic targets for mitigating PH progression.
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