Porphyromonas gingivalis infection causes umbilical vein endothelial barrier dysfunction in vitro by down-regulating ZO-1, occludin and VE-cadherin expression.
10.12122/j.issn.1673-4254.2023.02.18
- Author:
Jiao ZENG
1
;
Xin Zhu LI
1
;
Lin Ying YIN
1
;
Ting CHEN
1
;
Jin HOU
1
Author Information
1. Department of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
- Publication Type:Journal Article
- Keywords:
Porphyromonas gingivalis;
cell junction proteins;
endothelial barrier;
periodontitis;
umbilical vein endothelial cells
- MeSH:
Humans;
Cadherins/metabolism*;
Escherichia coli/metabolism*;
Human Umbilical Vein Endothelial Cells/metabolism*;
Occludin;
Porphyromonas gingivalis/metabolism*;
Umbilical Veins/metabolism*
- From:
Journal of Southern Medical University
2023;43(2):287-293
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the molecular mechanisms of Porphyromonas gingivalis infection-induced umbilical vein endothelial barrier dysfunction in vitro.
METHODS:Human umbilical vein endothelial cells (HUVECs) were cultured in vitro, and after the formation of the endothelial barrier, the cells were infected with P. gingivals at a multiplicity of infection (MOI). The transepithelial electrical resistance (TEER) of the cell barrier was measured, and FITC-dextran trans-endothelial permeability assay and bacterial translocation assay were performed to assess the endothelial barrier function. The expression levels of cell junction proteins including ZO-1, occludin and VE-cadherin in the cells were examined by qRT-PCR and Western blotting.
RESULTS:In freshly seeded HUVECs, TEER increased until reaching the maximum on Day 5 (94 Ωcm2), suggesting the formation of the endothelial barrier. P. gingivals infection caused an increase of the permeability of the endothelial barrier as early as 0.5 h after bacterial inoculation, and the barrier function further exacerbated with time, as shown by significantly lowered TEER, increased permeability of FITC-dextran (40 000/70 000), and increased translocation of SYTO9-E. coli cross the barrier. MTT assay suggested that P. gingivals infection did not significantly affect the proliferation of HUVECs (P>0.05), but in P. gingivalsinfected cells, the expressions of ZO-1, occludin and VE-cadherin increased significantly at 24 and 48 h after bacterial inoculation (P < 0.05).
CONCLUSION:P. gingivals may disrupt the endothelial barrier function by down-regulating the expressions of the cell junction proteins (ZO-1, occludin, VE-cadherin) and increasing the permeability of the endothelial barrier.
