ArticleAmerican journal of physiology. Lung cellular and molecular physiology2026
Endothelial-derived extracellular vesicles impair human pulmonary microvascular cell function in an in vitro model of sepsis-induced acute lung injury.
Article in American journal of physiology. Lung cellular and molecular physiology, 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
Acute respiratory distress syndrome (ARDS) remains a critical condition associated with high morbidity and mortality, particularly when triggered by sepsis. Endothelial dysfunction is a central hallmark of ARDS pathology, but the precise mechanisms underlying pulmonary microvascular dysfunction remain poorly understood. Extracellular vesicles (EVs) have emerged as crucial mediators of cell-cell communication during inflammation; however, their role in endothelial dysfunction in ARDS is less clearly defined. We utilized a human pulmonary microvascular endothelial cell (HPMEC)-based model of sepsis-induced acute lung injury to investigate whether inflammatory EVs (iEVs), derived from endothelial cells treated with bacterial lipopolysaccharide (LPS), impair naïve HPMEC function. EVs were characterized by nanoparticle tracking analysis, transmission electron microscopy, and immunofluorescence, confirming purity and uptake. iEV exposure significantly reduced barrier integrity by electric cell-substrate impedance sensing (ECIS) and increased cell migration; effects partially reversed by the toll-like receptor 4 (TLR4) inhibitor TAK-242. Adhesion and tube formation were unaffected. Pretreatment of donor HPMECs with the neutral sphingomyelinase inhibitor GW4869 attenuated the barrier-disrupting capacity of the resulting iEVs, implicating ceramide-dependent EV biogenesis in generating pathogenic cargo. Trypan Blue staining confirmed that these effects reflect altered signaling rather than cell death. iEV exposure upregulated TLR4, MyD88, interleukin-6 (IL-6), intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), E-selectin, and
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