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Coronary Artery Disease: HELP
Articles by Meng-Ling Wu
Based on 1 article published since 2010
(Why 1 article?)
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Between 2010 and 2020, Meng-Ling Wu wrote the following article about Coronary Artery Disease.
 
+ Citations + Abstracts
1 Article A Novel Protective Function of 5-Methoxytryptophan in Vascular Injury. 2016

Ho, Yen-Chun / Wu, Meng-Ling / Su, Chen-Hsuan / Chen, Chung-Huang / Ho, Hua-Hui / Lee, Guan-Lin / Lin, Wei-Shiang / Lin, Wen-Yu / Hsu, Yu-Juei / Kuo, Cheng-Chin / Wu, Kenneth K / Yet, Shaw-Fang. ·Institute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan. · Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan. · National Institute of Environmental Health Sciences, National Health Research Institutes, Zhunan, Taiwan. · Division of Cardiology, Department of Medicine, Tri-Service General Hospital, Taipei, Taiwan. · Division of Nephrology, Department of Medicine, Tri-Service General Hospital, Taipei, Taiwan. · Metabolomic Research Center and Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan. · Department of Medical Sciences and Institute of Biotechnology, National Tsing Hua University, Hsinchu, Taiwan. ·Sci Rep · Pubmed #27146795.

ABSTRACT: 5-Methoxytryptophan (5-MTP), a 5-methoxyindole metabolite of tryptophan metabolism, was recently shown to suppress inflammatory mediator-induced cancer cell proliferation and migration. However, the role of 5-MTP in vascular disease is unknown. In this study, we investigated whether 5-MTP protects against vascular remodeling following arterial injury. Measurements of serum 5-MTP levels in healthy subjects and patients with coronary artery disease (CAD) showed that serum 5-MTP concentrations were inversely correlated with CAD. To test the role of 5-MTP in occlusive vascular disease, we subjected mice to a carotid artery ligation model of neointima formation and treated mice with vehicle or 5-MTP. Compared with vehicle-treated mice, 5-MTP significantly reduced intimal thickening by 40% 4 weeks after ligation. BrdU incorporation assays revealed that 5-MTP significantly reduced VSMC proliferation both in vivo and in vitro. Furthermore, 5-MTP reduced endothelial loss and detachment, ICAM-1 and VCAM-1 expressions, and inflammatory cell infiltration in the ligated arterial wall, suggesting attenuation of endothelial dysfunction. Signaling pathway analysis indicated that 5-MTP mediated its effects predominantly via suppressing p38 MAPK signaling in endothelial and VSMCs. Our data demonstrate a novel vascular protective function of 5-MTP against arterial injury-induced intimal hyperplasia. 5-MTP might be a therapeutic target for preventing and/or treating vascular remodeling.