Oral diseases · 2026
Exosomes of Porphyromonas gingivalis-Infected Macrophages Impair the Endothelial Barrier and Angiogenesis In Vitro.
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Zhou Yanling, Huang Yihua, Lv Xiaomin, Liang Ailin, Liu Wenxuan, Tong Zhongchun, Gong Qimei
Аннотация
OBJECTIVES: Endothelial dysfunction is a key contributor to periodontal disease and apical periodontitis. However, the role of macrophages in mediating endothelial function via exosomes in these inflammatory diseases remains elusive.
MATERIALS AND METHODS: Exosomes isolated from Porphyromonas gingivalis (P.g)-infected THP-1-derived macrophages (P.g-Exos) and uninfected macrophages (Con-Exos) were verified and their effects on human umbilical vein endothelial cells (HUVECs) were investigated. The expression of TNF-α and IL-6 in HUVECs was tested by quantitative real time PCR (qRT-PCR) and ELISA. A fluorescein isothiocyanate (FITC)-dextran leakage assay and a THP-1 monocyte adhesion assay were used to explore vascular permeability and cellular adhesion. The migration and angiogenic capacity were evaluated using transwell, cell scratch, and tube-forming assays. HUVECs were pretreated with SC79 (Akt activator) to explore the mechanism.
RESULTS: P.g stimulation increased the release of exosomes from macrophages. P.g-Exos inhibited HUVECs' migration and tube formation capabilities while increasing vascular permeability, promoting leukocyte adhesion and releasing proinflammatory factors. Importantly, P.g-Exos induced endothelial dysfunction partially via the Akt/mTOR pathway suppression.
CONCLUSIONS: Summarily, this study reveals that the exosomes derived from inflammatory macrophages mediate HUVECs dysfunction partially via the Akt/mTOR pathway, providing novel insights into potential treatments for oral inflammatory diseases.
MATERIALS AND METHODS: Exosomes isolated from Porphyromonas gingivalis (P.g)-infected THP-1-derived macrophages (P.g-Exos) and uninfected macrophages (Con-Exos) were verified and their effects on human umbilical vein endothelial cells (HUVECs) were investigated. The expression of TNF-α and IL-6 in HUVECs was tested by quantitative real time PCR (qRT-PCR) and ELISA. A fluorescein isothiocyanate (FITC)-dextran leakage assay and a THP-1 monocyte adhesion assay were used to explore vascular permeability and cellular adhesion. The migration and angiogenic capacity were evaluated using transwell, cell scratch, and tube-forming assays. HUVECs were pretreated with SC79 (Akt activator) to explore the mechanism.
RESULTS: P.g stimulation increased the release of exosomes from macrophages. P.g-Exos inhibited HUVECs' migration and tube formation capabilities while increasing vascular permeability, promoting leukocyte adhesion and releasing proinflammatory factors. Importantly, P.g-Exos induced endothelial dysfunction partially via the Akt/mTOR pathway suppression.
CONCLUSIONS: Summarily, this study reveals that the exosomes derived from inflammatory macrophages mediate HUVECs dysfunction partially via the Akt/mTOR pathway, providing novel insights into potential treatments for oral inflammatory diseases.