Lysophosphatidylcholine up-regulates human endothelial nitric oxide synthase gene transactivity by c-Jun N-terminal kinase signalling pathway
Correction(s) for this article
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Erratum
- Volume 13Issue 9bJournal of Cellular and Molecular Medicine
- pages: 4084-4084
- First Published online: January 29, 2010
Corresponding Author
Feiyue Xing
Department of Biochemistry and Molecular Biology, Jinan University Guangzhou, China
Key Laboratory of Functional Proteomics of Guangdong Province and Key Laboratory for Shock and Microcirculation of Guangdong Province, Department of Pathophysiology the Southern Medical University, Guangzhou, China
Correspondence to: Feiyue XING, Kesen ZHAO, and Yong JIANG, Department of Biochemistry and Molecular Biology, College of Life Science and Technology, Jinan University, Guangzhou 510632 and Department of Pathophysiology, the Southern Medical University, Guangzhou, 510515, China. E-mail: [email protected], [email protected], and [email protected]Search for more papers by this authorJing Liu
Department of Stomatology, Jinan University, Guangzhou, China
Search for more papers by this authorYongyan Mo
Key Laboratory of Functional Proteomics of Guangdong Province and Key Laboratory for Shock and Microcirculation of Guangdong Province, Department of Pathophysiology the Southern Medical University, Guangzhou, China
Search for more papers by this authorZhifeng Liu
Key Laboratory of Functional Proteomics of Guangdong Province and Key Laboratory for Shock and Microcirculation of Guangdong Province, Department of Pathophysiology the Southern Medical University, Guangzhou, China
Search for more papers by this authorQinghe Qin
Key Laboratory of Functional Proteomics of Guangdong Province and Key Laboratory for Shock and Microcirculation of Guangdong Province, Department of Pathophysiology the Southern Medical University, Guangzhou, China
Search for more papers by this authorJingzhen Wang
Key Laboratory of Functional Proteomics of Guangdong Province and Key Laboratory for Shock and Microcirculation of Guangdong Province, Department of Pathophysiology the Southern Medical University, Guangzhou, China
Search for more papers by this authorZhenhua Fan
Department of Biochemistry and Molecular Biology, Jinan University Guangzhou, China
Search for more papers by this authorYutian Long
Department of Biochemistry and Molecular Biology, Jinan University Guangzhou, China
Search for more papers by this authorNa Liu
Department of Biochemistry and Molecular Biology, Jinan University Guangzhou, China
Search for more papers by this authorCorresponding Author
Kesen Zhao
Key Laboratory of Functional Proteomics of Guangdong Province and Key Laboratory for Shock and Microcirculation of Guangdong Province, Department of Pathophysiology the Southern Medical University, Guangzhou, China
Correspondence to: Feiyue XING, Kesen ZHAO, and Yong JIANG, Department of Biochemistry and Molecular Biology, College of Life Science and Technology, Jinan University, Guangzhou 510632 and Department of Pathophysiology, the Southern Medical University, Guangzhou, 510515, China. E-mail: [email protected], [email protected], and [email protected]Search for more papers by this authorCorresponding Author
Yong Jiang
Key Laboratory of Functional Proteomics of Guangdong Province and Key Laboratory for Shock and Microcirculation of Guangdong Province, Department of Pathophysiology the Southern Medical University, Guangzhou, China
Correspondence to: Feiyue XING, Kesen ZHAO, and Yong JIANG, Department of Biochemistry and Molecular Biology, College of Life Science and Technology, Jinan University, Guangzhou 510632 and Department of Pathophysiology, the Southern Medical University, Guangzhou, 510515, China. E-mail: [email protected], [email protected], and [email protected]Search for more papers by this authorCorresponding Author
Feiyue Xing
Department of Biochemistry and Molecular Biology, Jinan University Guangzhou, China
Key Laboratory of Functional Proteomics of Guangdong Province and Key Laboratory for Shock and Microcirculation of Guangdong Province, Department of Pathophysiology the Southern Medical University, Guangzhou, China
Correspondence to: Feiyue XING, Kesen ZHAO, and Yong JIANG, Department of Biochemistry and Molecular Biology, College of Life Science and Technology, Jinan University, Guangzhou 510632 and Department of Pathophysiology, the Southern Medical University, Guangzhou, 510515, China. E-mail: [email protected], [email protected], and [email protected]Search for more papers by this authorJing Liu
Department of Stomatology, Jinan University, Guangzhou, China
Search for more papers by this authorYongyan Mo
Key Laboratory of Functional Proteomics of Guangdong Province and Key Laboratory for Shock and Microcirculation of Guangdong Province, Department of Pathophysiology the Southern Medical University, Guangzhou, China
Search for more papers by this authorZhifeng Liu
Key Laboratory of Functional Proteomics of Guangdong Province and Key Laboratory for Shock and Microcirculation of Guangdong Province, Department of Pathophysiology the Southern Medical University, Guangzhou, China
Search for more papers by this authorQinghe Qin
Key Laboratory of Functional Proteomics of Guangdong Province and Key Laboratory for Shock and Microcirculation of Guangdong Province, Department of Pathophysiology the Southern Medical University, Guangzhou, China
Search for more papers by this authorJingzhen Wang
Key Laboratory of Functional Proteomics of Guangdong Province and Key Laboratory for Shock and Microcirculation of Guangdong Province, Department of Pathophysiology the Southern Medical University, Guangzhou, China
Search for more papers by this authorZhenhua Fan
Department of Biochemistry and Molecular Biology, Jinan University Guangzhou, China
Search for more papers by this authorYutian Long
Department of Biochemistry and Molecular Biology, Jinan University Guangzhou, China
Search for more papers by this authorNa Liu
Department of Biochemistry and Molecular Biology, Jinan University Guangzhou, China
Search for more papers by this authorCorresponding Author
Kesen Zhao
Key Laboratory of Functional Proteomics of Guangdong Province and Key Laboratory for Shock and Microcirculation of Guangdong Province, Department of Pathophysiology the Southern Medical University, Guangzhou, China
Correspondence to: Feiyue XING, Kesen ZHAO, and Yong JIANG, Department of Biochemistry and Molecular Biology, College of Life Science and Technology, Jinan University, Guangzhou 510632 and Department of Pathophysiology, the Southern Medical University, Guangzhou, 510515, China. E-mail: [email protected], [email protected], and [email protected]Search for more papers by this authorCorresponding Author
Yong Jiang
Key Laboratory of Functional Proteomics of Guangdong Province and Key Laboratory for Shock and Microcirculation of Guangdong Province, Department of Pathophysiology the Southern Medical University, Guangzhou, China
Correspondence to: Feiyue XING, Kesen ZHAO, and Yong JIANG, Department of Biochemistry and Molecular Biology, College of Life Science and Technology, Jinan University, Guangzhou 510632 and Department of Pathophysiology, the Southern Medical University, Guangzhou, 510515, China. E-mail: [email protected], [email protected], and [email protected]Search for more papers by this authorAbstract
Human endothelial nitric oxide synthase (eNOS) plays a pivotal role in maintaining blood pressure homeostasis and vascular integrity. It has recently been reported that mitogen-activated protein kinases (MAPKs) are intimately implicated in expression of eNOS. However detailed mechanism mediated by them remains to be clarified. In this study, eNOS gene transactivity in human umbilical vein endothelial cells was up-regulated by stimulation of lysophosphatidylcholine (LPC). The stimulation of LPC highly activated both extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK), with differences in the dynamic processes of activation between them. Unexpectedly, p38 MAPK could not be activated by the stimulation of LPC. The activation of JNK signalling pathway by overexpression of JNK or its upstream kinase active mutant up-regulated the transactivity of eNOS significantly, but the activation of p38 signalling pathway down-regulated it largely. The inhibition of either ERK1/2 or JNK signalling pathway by kinase-selective inhibitors could markedly block the induction of the transactivity by LPC. It was observed by electrophoretic mobility shift assay that LPC stimulated both SP1 and AP1 DNA binding activity to go up. Additionally using decoy oligonucleotides proved that SP1 was necessary for maintaining the basal or stimulated transactivity, whereas AP1 contributed mainly to the increase of the stimulated transactivity. These findings indicate that the up-regulation of the eNOS gene transactivity by LPC involves the enhancement of SP1 transcription factor by the activation of JNK and ERK1/2 signalling pathways and AP1 transcription factor by the activation of JNK signalling pathway.
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