title: 5-Methoxytryptophan-dependent protection of cardiomyocytes from heart ischemia reperfusion injury.
abstract: 5-Methoxytryptophan (5-MTP), a catabolic product of tryptophan, can block Cox-2 overexpression in cancer cells as well as suppress cancer cell growth, migration and invasion. The aim of this study was to in vitro examine whether 5-MTP is able to reduce reactive oxygen species (ROS)-induced heart ischemia reperfusion injury and activate the cardiomyocyte's damage surveillance systems. Accordingly, rattus cardiomyocytes were treated with H2O2 as a heart ischemia reperfusion model prior to incubation with/without 5-MTP and proteomic analysis was performed to investigate the physiologic protection of 5-MTP in H2O2-induced ischemia reperfusion in cardiomyocyte. Our data demonstrated that 5-MTP treatment does protect cardiomyocyte in the ROS-induced ischemia reperfusion model. 5-MTP has also been shown to significantly facilitate cell migration and wound healing via cytoskeletal regulations. Additionally, two-dimensional differential gel electrophoresis (2D-DIGE) combined matrix assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF/TOF MS) analysis showed that 5-MTP might modulate growth-associated proteins, cytoskeleton regulation, redox regulation and protein folding to stimulate wound healing as well as prevent these ischemia reperfusion-damaged cardiomyocytes from cell death through maintaining cellular redox-balance and reducing ER-stress. To our knowledge, we report for the first time the cell repair mechanism of 5-MTP against ischemia reperfusion-damage in cardiomyocytes based on cell biology and proteomic analysis.
authors.affiliation: Department of Applied Science, National Hsinchu University of Education, Hsinchu, Taiwan.
authors.forename: Hsiu-Chuan
authors.initials: HC
authors.lastname: Chou
authors.affiliation: Institute of Bioinformatics and Structural Biology & Department of Medical Sciences, National Tsing Hua University, Hsinchu, Taiwan. Electronic address: hlchan@life.nthu.edu.tw.
authors.forename: Hong-Lin
authors.initials: HL
authors.lastname: Chan
mesh_terms: D000818:Animals; D016923:Cell Death / Q000187:drug effects; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D019610:Cytoprotection / Q000187:drug effects*; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects; D006861:Hydrogen Peroxide / Q000494:pharmacology; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism* / Q000473:pathology; D040901:Proteomics; D051381:Rats; D015427:Reperfusion Injury / Q000235:genetics / Q000378:metabolism / Q000473:pathology* / Q000517:prevention & control*; D059467:Transcriptome / Q000187:drug effects; D014364:Tryptophan / Q000031:analogs & derivatives* / Q000494:pharmacology
chemical_list: C027986:5-methoxytryptophan; D014364:Tryptophan; D006861:Hydrogen Peroxide
keywords: 5-Methoxytryptophan; Cardiomyocytes; DIGE; Ischemia reperfusion injury; Oxidative stress; Proteomics