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Title of the item:

Amine oxidase 3 is a novel pro-inflammatory marker of oxidative stress in peritoneal endometriosis lesions

Title :
Amine oxidase 3 is a novel pro-inflammatory marker of oxidative stress in peritoneal endometriosis lesions
Authors :
Marie-Laëtitia Thézénas
Bianca De Leo
Alexis Laux-Biehlmann
Cemsel Bafligil
Bernd Elger
Thomas Tapmeier
Karl Morten
Nilufer Rahmioglu
Stephanie G. Dakin
Philip Charles
Fernando Estrada Martinez
Graham Steers
Oliver M. Fischer
Joerg Mueller
Holger Hess-Stumpp
Andreas Steinmeyer
Sanjiv Manek
Krina T. Zondervan
Stephen Kennedy
Christian M. Becker
Catherine Shang
Thomas M. Zollner
Benedikt M. Kessler
Udo Oppermann
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Subject Terms :
Source :
Scientific Reports, Vol 10, Iss 1, Pp 1-11 (2020)
Publisher :
Nature Publishing Group, 2020.
Publication Year :
Collection :
Document Type :
File Description :
electronic resource
Language :
Relation :;
Access URL :
Accession Number :
Academic Journal
Abstract Endometriosis is a common gynaecological disease of women in reproductive age, and is thought to arise from retrograde menstruation and implantation of endometrial tissue, mostly into the peritoneal cavity. The condition is characterized by a chronic, unresolved inflammatory process thereby contributing to pain as cardinal symptom in endometriosis. Elevated reactive oxygen species (ROS) and oxidative stress have been postulated as factors in endometriosis pathogenesis. We here set out for a systematic study to identify novel mechanisms and pathways relating to oxidative stress in ectopic peritoneal lesions. Using combined proteomic and transcriptomic approaches, we identified novel targets including upregulated pro-oxidative enzymes, such as amine oxidase 3/vascular adhesion protein 1 (AOC3/VAP1) as well as downregulated protective factors, in particular alkenal reductase PTGR1 and methionine sulfoxide reductase. Consistent with an altered ROS landscape, we observed hemoglobin / iron overload, ROS production and lipid peroxidation in ectopic lesions. ROS-derived 4-hydroxy-2-nonenal induced interleukin IL-8 release from monocytes. Notably, AOC3 inhibitors provoked analgesic effects in inflammatory pain models in vivo, suggesting potential translational applicability.
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