The Adhesion GPCR GPR125 is specifically expressed in the choroid plexus and is upregulated following brain injury

• Autor(a) principal: Pickering, Chris
• Data de Publicação: 2008
• Outros Autores: Hägglund, Maria, Szmydynger-Chodobska, Joanna, Marques, Fernanda, Palha, Joana Almeida, Waller, Linn, Chodobski, Adam, Fredriksson, Robert, Lagerström, Malin C., Schiöth, Helgi B.
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• Texto Completo: http://hdl.handle.net/1822/58826
• topic: Animals; Base Sequence; Brain Injuries; Choroid Plexus; Gene Expression Profiling; Hippocampus; Humans; Immunohistochemistry; In Situ Hybridization; Inflammation; Keratins; Lipopolysaccharides; Male; Membrane Glycoproteins; Membrane Proteins; Mice; Platelet Glycoprotein GPIb-IX Complex; RNA, Messenger; Rats; Receptors, G-Protein-Coupled; Time Factors; Up-Regulation; Science & Technology

Background: GPR125 belongs to the family of Adhesion G protein-coupled receptors (GPCRs). A single copy of GPR125 was found in many vertebrate genomes. We also identified a Drosophila sequence, DmCG15744, which shares a common ancestor with the entire Group III of Adhesion GPCRs, and also contains Ig, LRR and HBD domains which were observed in mammalian GPR125.Results: We found specific expression of GPR125 in cells of the choroid plexus using in situ hybridization and protein-specific antibodies and combined in situ/immunohistochemistry co-localization using cytokeratin, a marker specific for epithelial cells. Induction of inflammation by LPS did not change GPR125 expression. However, GPR125 expression was transiently increased ( almost 2-fold) at 4 h after traumatic brain injury (TBI) followed by a decrease ( approximately 4-fold) from 2 days onwards in the choroid plexus as well as increased expression ( 2-fold) in the hippocampus that was delayed until 1 day after injury.Conclusion: These findings suggest that GPR125 plays a functional role in choroidal and hippocampal response to injury.