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Published on: August 8, 2014
Exosomes of Porphyromonas gingivalis-Infected Macrophages Impair the Endothelial Barrier and Angiogenesis In Vitro
Yanling Zhou1,2,3, Yihua Huang1,2,3, Xiaomin Lv1,2,3
1Hosiptal of Stomatology, Sun Yat-Sen University, Guangzhou, Guangdong, China.
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.
Insights
Exosomes from Porphyromonas gingivalis-infected macrophages cause endothelial dysfunction by suppressing the Akt/mTOR pathway, offering new therapeutic targets for oral inflammatory diseases.
Area of Science:
- Oral biology and immunology
- Endothelial cell biology
- Exosome biology
Background:
- Endothelial dysfunction is central to periodontal disease and apical periodontitis.
- The role of macrophage-derived exosomes in these conditions is not well understood.
Purpose of the Study:
- To investigate the impact of exosomes from Porphyromonas gingivalis-infected macrophages on endothelial cells.
- To elucidate the underlying molecular mechanisms of exosome-mediated endothelial dysfunction.
Main Methods:
- Isolation and verification of exosomes from infected (P.g-Exos) and uninfected (Con-Exos) macrophages.
- Assessment of P.g-Exos effects on human umbilical vein endothelial cells (HUVECs) including permeability, adhesion, migration, and angiogenesis.
- Analysis of inflammatory marker expression (TNF-α, IL-6) and investigation of the Akt/mTOR pathway.
Main Results:
- P.g-Exos inhibited HUVEC migration and angiogenesis, increased vascular permeability, and promoted leukocyte adhesion.
- P.g-Exos induced the release of pro-inflammatory factors from HUVECs.
- Endothelial dysfunction induced by P.g-Exos was partially mediated by the suppression of the Akt/mTOR pathway.
Conclusions:
- Exosomes derived from inflammatory macrophages contribute to endothelial dysfunction in oral inflammatory diseases.
- Targeting the Akt/mTOR pathway offers a potential therapeutic strategy for these conditions.
- This study provides novel insights into the pathogenesis of oral inflammatory diseases and potential treatment avenues.
