Jilin Li1, Shuying Chen1, Xiangna Cai2, Huaiwen Wang3, Xin Wang1, Wei Wang3. 1. Department of Interventional cardiology, First Affiliated Hospital of Shantou University Medical College Shantou, Guangdong Province, China. 2. Department of Plastic Surgeon, First Affiliated Hospital of Shantou University Medical College Shantou, Guangdong Province, China. 3. Department of Cardiology, Second Affiliated Hospital of Shantou University Medical College Shantou, Guangdong Province, China.
Abstract
BACKGROUND: Inflammatory responses induced by ox-LDL play important roles in atherogenesis, and could be promoted in diabetic patients. Toll-like receptor (TLR)2 is an innate inflammatory receptor, and is enhanced in human umbilical vein endothelial cells (HUVECs) under high glucose conditions. Ox-LDL-TLR2 pathway activation and further inflammation in monocytes are involved in the atherosclerosis formation. OBJECTIVE: What role of TLR2 plays on ox-LDL-induced inflammation in HUVECs remains unclear, especially in high glucose conditions. The purpose of this study is to explore the effect and role of ox-LDL-TLR2 pathway on the inflammatory responses in HUVECs. METHODS: 1 hour prior to the treatment, HUVECs were treated with or without neutralizing anti-TLR2 antibody. After that, HUVECs were treated with ox-LDL (20, or 40 μg/ml) or LPS (200 ng/ml) under normal and high glucose conditions. The expressions of ICAM-1 and TLR2 protein were analyzed by immunoblotting, and IL-6 and IL-8 were measured by ELISA. RESULTS: Compared with those in normal glucose condition, IL-6 and IL-8 expression were increased in high glucose condition. The stimulation of ox-LDL and LPS both increased the expression of ICAM-1, IL-6 and IL-8, but did not change TLR2 protein expression in both normal and high glucose conditions. Additionally, the expression of ICAM-1, IL-6 and IL-8 was not changed when TLR2 was knocked out under these two conditions. CONCLUSION: The inflammatory responses induced by Ox-LDL were not changed with or without TLR2 under both normal and high glucose conditions in HUVECs. Our study indicates TLR2 is not involved in the ox-LDL mediated endothelial injury under high glucose conditions, which is an important step of atherosclerosis formation in diabetes.
BACKGROUND: Inflammatory responses induced by ox-LDL play important roles in atherogenesis, and could be promoted in diabeticpatients. Toll-like receptor (TLR)2 is an innate inflammatory receptor, and is enhanced in human umbilical vein endothelial cells (HUVECs) under high glucose conditions. Ox-LDL-TLR2 pathway activation and further inflammation in monocytes are involved in the atherosclerosis formation. OBJECTIVE: What role of TLR2 plays on ox-LDL-induced inflammation in HUVECs remains unclear, especially in high glucose conditions. The purpose of this study is to explore the effect and role of ox-LDL-TLR2 pathway on the inflammatory responses in HUVECs. METHODS: 1 hour prior to the treatment, HUVECs were treated with or without neutralizing anti-TLR2 antibody. After that, HUVECs were treated with ox-LDL (20, or 40 μg/ml) or LPS (200 ng/ml) under normal and high glucose conditions. The expressions of ICAM-1 and TLR2 protein were analyzed by immunoblotting, and IL-6 and IL-8 were measured by ELISA. RESULTS: Compared with those in normal glucose condition, IL-6 and IL-8 expression were increased in high glucose condition. The stimulation of ox-LDL and LPS both increased the expression of ICAM-1, IL-6 and IL-8, but did not change TLR2 protein expression in both normal and high glucose conditions. Additionally, the expression of ICAM-1, IL-6 and IL-8 was not changed when TLR2 was knocked out under these two conditions. CONCLUSION: The inflammatory responses induced by Ox-LDL were not changed with or without TLR2 under both normal and high glucose conditions in HUVECs. Our study indicates TLR2 is not involved in the ox-LDL mediated endothelial injury under high glucose conditions, which is an important step of atherosclerosis formation in diabetes.