A key mediator, PTX3, of IKK/I kappa B/NF-kappa B exacerbates human umbilical vein endothelial cell injury and dysfunction

作者：Zhao, Yongbo; Feng, Guangxing^*; Wang, Yanzhi; Yue, Yuehong; Zhao, Weichao

来源：International Journal of Clinical and Experimental Pathology, 2014, 7(11): 7699-7707.

• PTX3
• NF-kappa B
• iNOS
• atherosclerosis
• HUVECs

Objective: This study was performed to investigate PTX3-mediated iNOS expression and IKK/I kappa B/NF-kappa B activation in PA-induced atherosclerotic HUVECs injury model. Methods: The cell viability was detected by the CCK8 assay. The cell apoptosis was assessed by annexin V-PI double-labeling staining. Expression of genes and proteins were analyzed by real-time PCR and western blotting respectively. Cells were transfected with siRNAs as a gene silencing methods. Results: PA induced cell apoptosis in human umbilical vein endothelial cells in a time and dose-dependent manner. PA also induced upregulation expression of PTX3. TPCA-1, an inhibitor of IKK-2, could suppress the expression of PTX3 and phospho-I kappa B-alpha in PA-induced endothelial dysfunction cell model. We also found that transfection of cells with PTX3 siRNA reduced the expression of iNOS and NO, and protected PA-induced cell apoptosis in HUVECs. Conclusions: PTX3 could exacerbate endothelial dysfunction, at least partially, through IKK/I kappa B/NF-kappa B activation and overexpression of iNOS and NO, and advance the development of atherosclerosis.

• 出版日期2014
• 单位河北省人民医院; 河北医科大学