Heat-shock protein 60 of Porphyromonas gingivalis may induce dysfunction of human umbilical endothelial cells via regulation of endothelial‑nitric oxide synthase and vascular endothelial‑cadherin

Wu,Cunjin; Guo,Shijie; Niu,Yuanjie; Yang,Limin; Liu,Bainian; Jiang,Ning; Su,Ming; Wang,Lin

doi:10.3892/br.2016.693

Heat-shock protein 60 of Porphyromonas gingivalis may induce dysfunction of human umbilical endothelial cells via regulation of endothelial‑nitric oxide synthase and vascular endothelial‑cadherin

Authors:
- Cunjin Wu
- Shijie Guo
- Yuanjie Niu
- Limin Yang
- Bainian Liu
- Ning Jiang
- Ming Su
- Lin Wang
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Affiliations: Department of Geratology, The Second Hospital of Tianjin Medical University, Tianjin 300211, P.R. China, Department of Urology, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin 300211, P.R. China, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, P.R. China
Published online on: May 27, 2016 https://doi.org/10.3892/br.2016.693
Pages: 243-247

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Abstract

Accumulating evidence has established that periodontitis was an independent risk factor for coronary heart disease (CAD). Porphyromonus gingivalis (P. gingivalis), a major periodontal pathogen, has already been shown to have a significant role in the inflammatory response of CAD in vivo. The aim of the present study was to identify whether P. gingivalis heat‑shock protein 60 (HSP60) induced the dysfunction of human umbilical vein endothelial cells (HUVECs) in vitro. HUVECs were stimulated with a range of P. gingivalis HSP60 concentrations (1, 10 and 100 ng/l) at different time‑points. The levels of vascular endothelial (VE)‑cadherin, endothelial nitric oxide synthase (eNOS) and cysteinyl aspartate‑specific protease‑3 (caspase‑3) were measured using western blot analysis. The apoptotic rate of HUVECs was detected using flow cytometry. P. gingivalis HSP60 at a concentration of 10 ng/l significantly decreased the expression levels of VE‑cadherin and eNOS protein at 24 h stimulation, whereas no difference in these proteins was identified following a low dose of P. gingivalis HSP60 (1 ng/l). P. gingivalis HSP60 at 100 ng/l significantly downregulated the expression levels of VE‑cadherin and eNOS protein at 12 h in HUVECs. However, the cleavage of caspase‑3 showed an opposing change at different concentrations. Consistently, P. gingivalis HSP60 induced apoptosis of HUVECs in a concentration‑dependent manner. These results indicated that P. gingivalis HSP60 may induce dysfunction and apoptosis in HUVECs via downregulating the expression levels of VE‑cadherin and eNOS, and promoting the cleavage of caspase‑3.

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