Role of sphingosine 1-phosphate on high glucose-induced vascular endothelial cell dysfunction |
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Authors: | LIU Wei-hua LIN Shuang-feng SHI Ji-xiang PAN Ting CHEN Qiu-mei WANG Shuo-ting SHANG Hui |
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Institution: | 1. The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease, Guangzhou 510260, China;
2. The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou 510405, China |
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Abstract: | AIM: To explore the role of sphingosine 1-phosphate (S1P) in the dysfunction of vascular endothelial cells exposed to high glucose. METHODS: In human aortic endothelial cells cultured under high-glucose (22 mmol/L glucose) medium, nitric oxide (NO) level, polymorphonuclear neutrophil-endothelial cell adhesion rate, protein level of intercellular adhesion molecule-1 (ICAM-1), migration of endothelial cells and Akt/endothelial nitric oxide synthase (eNOS) pathway activation were observed after S1P, sphingosine kinase-1 inhibitor and/or Akt inhibitor treatments. RESULTS: S1P decreased NO level, increased polymorphonuclear neutrophil adhesive rate, enhanced ICAM-1 protein level, and inhibited migration of endothelial cells and activation of Akt/eNOS pathway in endothelial cells cultured under high-glucose condition. Sphingosine kinase-1 inhibitor, which reduced S1P content, significantly improved the above endothelial cell function indexes and restored the activation of Akt/eNOS pathway. CONCLUSION: S1P promoted high glucose-induced dysfunction of endothelial cells probably by inhibiting the activation of Akt/eNOS signal pathway. Targeting S1P is expected to become one of potential treatment strategies to reduce endothelial cell dysfunction. |
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Keywords: | Sphingosine 1-phosphate Endothelial cells Endothelial nitric oxide synthase Intercellular adhesion molecule-1 |
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