| Content Provider |
World Health Organization (WHO)-Global Index Medicus |
| Author |
Sung, Li-Chin Chao, Hung-Hsing Chen, Cheng-Hsien Tsai, Jen-Chen Liu, Ju-Chi Hong, Hong-Jye Cheng, Tzu-Hurng Chen, Jin-Jer |
| Description |
Country affiliation: Taiwan Author Affiliation: Sung LC ( Division of Cardiology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.); Chao HH ( Shin Kong Wu Ho-Su Memorial Hospital, Taipei Medical University, Taipei, Taiwan.); Chen CH ( Department of Surgery, School of Medicine, Taipei Medical University, Taipei, Taiwan.); Tsai JC ( Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.); Liu JC ( Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.); Hong HJ ( Division of Cardiology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.); Cheng TH ( School of Chinese Medicine, China Medical University, Taichung, Taiwan.); Chen JJ ( Department of Biochemistry, School of Medicine, China Medical University, Taichung, Taiwan.) |
| Abstract |
Lycopene is the most potent active antioxidant among the major carotenoids, and its use has been associated with a reduced risk for cardiovascular disease (CVD). Endothelin-1 (ET-1) is a powerful vasopressor synthesized by endothelial cells and plays a crucial role in the pathophysiology of CVD. However, the direct effects of lycopene on vascular endothelial cells have not been fully described. This study investigated the effects of lycopene on cyclic strain-induced ET-1 gene expression in human umbilical vein endothelial cells (HUVECs) and identified the signal transduction pathways that are involved in this process. Cultured HUVECs were exposed to cyclic strain (20% in length, 1 Hz) in the presence or absence of lycopene. Lycopene inhibited strain-induced ET-1 expression through the suppression of reactive oxygen species (ROS) generation through attenuation of p22(phox) mRNA expression and NAD(P)H oxidase activity. Furthermore, lycopene inhibited strain-induced ET-1 secretion by reducing ROS-mediated extrace-llular signal-regulated kinase (ERK) phosphorylation. Conversely, lycopene treatment enhanced heme oxygenase-1 (HO-1) gene expression through the activation of phosphoinositide 3-kinase (PI3K)/Akt pathway, followed by induction of the nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation; in addition, HO-1 silencing partially inhibited the repressive effects of lycopene on strain-induced ET-1 expression. In summary, our study showed, for the first time, that lycopene inhibits cyclic strain-induced ET-1 gene expression through the suppression of ROS generation and induction of HO-1 in HUVECs. Therefore, this study provides new valuable insight into the molecular pathways that may contribute to the proposed beneficial effects of lycopene on the cardiovascular system. |
| File Format |
HTM / HTML |
| ISSN |
03051870 |
| Issue Number |
6 |
| Volume Number |
42 |
| e-ISSN |
14401681 |
| Journal |
Clinical and Experimental Pharmacology and Physiology |
| Language |
English |
| Publisher |
Wiley-Blackwell |
| Publisher Date |
2015-06-01 |
| Publisher Place |
Australia |
| Access Restriction |
One Nation One Subscription (ONOS) |
| Subject Keyword |
Discipline Physiology Discipline Pharmacology Carotenoids Pharmacology Endothelin-1 Biosynthesis Heme Oxygenase-1 Human Umbilical Vein Endothelial Cells Metabolism Reactive Oxygen Species Stress, Mechanical Cells, Cultured Dose-response Relationship, Drug Enzyme Induction Drug Effects Physiology Gene Expression Regulation Humans Journal Article Research Support, Non-u.s. Gov't |
| Content Type |
Text |
| Resource Type |
Article |
| Subject |
Physiology Physiology (medical) Pharmacology |
