Peri-Infarct Upregulation of the Oxytocin Receptor in Vascular Dementia.
Alzheimer disease
Astrocvytes
Microinfarcts
Microvascular endothelial cells
Oxytocin receptor
Vascular dementia
Journal
Journal of neuropathology and experimental neurology
ISSN: 1554-6578
Titre abrégé: J Neuropathol Exp Neurol
Pays: England
ID NLM: 2985192R
Informations de publication
Date de publication:
01 05 2019
01 05 2019
Historique:
entrez:
17
4
2019
pubmed:
17
4
2019
medline:
13
6
2020
Statut:
ppublish
Résumé
Vascular dementia (VaD) is cognitive decline linked to reduced cerebral blood perfusion, yet there are few therapeutic options to protect cognitive function following cerebrovascular accidents. The purpose of this study was to profile gene expression changes unique to VaD to identify and characterize disease relevant changes that could offer clues for future therapeutic direction. Microarray-based profiling and validation studies of postmortem frontal cortex samples from VaD, Alzheimer disease, and age-matched control subjects revealed that the oxytocin receptor (OXTR) was strongly and differentially upregulated in VaD. Further characterization in fixed tissue from the same cases showed that OXTR upregulation occurs de novo around and within microinfarcts in peri-infarct reactive astrocytes as well as within vascular profiles, likely on microvascular endothelial cells. These results indicate that increased OXTR expression in peri-infarct regions may be a specific response to microvascular insults. Given the established OXTR signaling cascades that elicit antioxidant, anti-inflammatory, and pro-angiogenic responses, the present findings suggest that de novo OXTR expression in the peri-infarct space is a tissue-protective response by astroglial and vascular cells in the wake of ischemic damage that could be exploited as a therapeutic option for the preservation of cognition following cerebrovascular insults.
Identifiants
pubmed: 30990880
pii: 5445920
doi: 10.1093/jnen/nlz023
pmc: PMC6467199
doi:
Substances chimiques
Receptors, Oxytocin
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
436-452Subventions
Organisme : NIA NIH HHS
ID : P01 AG014449
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG053760
Pays : United States
Organisme : NIA NIH HHS
ID : R21 AG053581
Pays : United States
Informations de copyright
© 2019 American Association of Neuropathologists, Inc. All rights reserved.
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