A scavenger peptide prevents methylglyoxal induced pain in mice

The reactive metabolite methylglyoxal (MG) has been identified as mediator of pain. Scavenging of free MG and the prevention of MG-derived post-translational modifications may provide a useful therapeutic treatment. An arginine-rich, fatty acid coupled, cyclic peptide (CycK(Myr)R4E) with high proteo...

Full description

Saved in:
Bibliographic Details
Main Authors: Brings, Sebastian (Author) , Fleming, Thomas (Author) , Beijer, Barbro (Author) , Lindner, Thomas (Author) , Wischnjow, Artjom (Author) , Kender, Zoltán (Author) , Peters, Verena (Author) , Kopf, Stefan (Author) , Haberkorn, Uwe (Author) , Mier, Walter (Author) , Nawroth, Peter Paul (Author)
Format: Article (Journal)
Language:English
Published: 2017
In: Biochimica et biophysica acta. Molecular basis of disease
Year: 2017, Volume: 1863, Issue: 3, Pages: 654-662
ISSN:1879-260X
DOI:10.1016/j.bbadis.2016.12.001
Online Access:Volltext
Volltext
Get full text
Author Notes:Sebastian Brings, Thomas Fleming, Svenja De Buhr, Barbro Beijer, Thomas Lindner, Artjom Wischnjow, Zoltan Kender, Verena Peters, Stefan Kopf, Uwe Haberkorn, Walter Mier, Peter P. Nawroth
Description
Summary:The reactive metabolite methylglyoxal (MG) has been identified as mediator of pain. Scavenging of free MG and the prevention of MG-derived post-translational modifications may provide a useful therapeutic treatment. An arginine-rich, fatty acid coupled, cyclic peptide (CycK(Myr)R4E) with high proteolytic stability and prolonged circulation was developed for the scavenging of MG. It was shown to reduce the formation of albumin-MG adducts in vitro and prevented MG-induced pain by reducing plasma MG levels through the formation of peptide-MG adducts in vivo. CycK(Myr)R4E therefore presents a promising option for the treatment of pain and other diabetic complications associated with high MG levels.
Item Description:Available online: 6 December 2016
Gesehen am 19.07.2018
Physical Description:Online Resource
ISSN:1879-260X
DOI:10.1016/j.bbadis.2016.12.001