bromochloroacetic-acid and Brain-Injuries

Topics: Acrylic Resins; Adsorption; Animals; Behavior, Animal; Brain; Brain Injuries; Cerebral Hemorrhage; Deferoxamine; Disease Models, Animal; Drug Liberation; Hydrogels; Iron; Keratins; Male; Rats, Sprague-Dawley; Siderophores; Temperature

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.. 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.. These findings suggest that GPR125 plays a functional role in choroidal and hippocampal response to injury.

Topics: 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; Rats; Receptors, G-Protein-Coupled; RNA, Messenger; Time Factors; Up-Regulation

Surgical brain injury causes neovascularization in the disrupted brain parenchyma, which occurs with the participation of endothelial-like cells. Differentiation of angioblasts from embryonic mesothelial cells has been proposed on the ground of biochemical and antigenic similarities between mesothelial and endothelial cells. Therefore, a transient localization of cytokeratin, the main mesothelial intermediate filament protein, to some embryonic vessels and endothelial progenitors, prompted us to use it to identify the source of cells participating in vessel formation after surgical brain injury. To determine the immunophenotypes of immature endothelial cells involved in new vessel formation following surgical rat brain injury, we used immunohistochemical and electron microscopic immunocytochemical techniques. Subcellular localization of protein markers: Flk-1, cytokeratin, and vimentin was examined in the cells investigated. Our results confirmed the existence of a diversity of immunophenotypes of immature endothelial cells in case of surgical-related brain injury.

Topics: AC133 Antigen; Animals; Antigens, CD; Brain Injuries; Cell Lineage; Cerebral Cortex; Disease Models, Animal; Endothelial Cells; Glycoproteins; Immunohistochemistry; Immunophenotyping; Keratins; Male; Microscopy, Immunoelectron; Neovascularization, Physiologic; Peptides; Rats; Rats, Wistar; Time Factors; Vascular Endothelial Growth Factor Receptor-2; Vimentin