Yongbo Zhao1, Guangxing Feng1, Yanzhi Wang1, Yuehong Yue2, Weichao Zhao1. 1. Department of Cardiovascular Surgery, Fourth Hospital of Hebei Medical University Shijiazhuang, China. 2. Department of Neurology, Hebei General Hospital Shijiazhuang, China.
Abstract
OBJECTIVE: This study was performed to investigate PTX3-mediated iNOS expression and IKK/IκB/NF-κB 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-IκB-α 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/IκB/NF-κB activation and overexpression of iNOS and NO, and advance the development of atherosclerosis.
OBJECTIVE: This study was performed to investigate PTX3-mediated iNOS expression and IKK/IκB/NF-κB 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-IκB-α 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/IκB/NF-κB activation and overexpression of iNOS and NO, and advance the development of atherosclerosis.
Authors: G Peri; M Introna; D Corradi; G Iacuitti; S Signorini; F Avanzini; F Pizzetti; A P Maggioni; T Moccetti; M Metra; L D Cas; P Ghezzi; J D Sipe; G Re; G Olivetti; A Mantovani; R Latini Journal: Circulation Date: 2000-08-08 Impact factor: 29.690