FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2156165184> ?p ?o ?g. }

• W2156165184 abstract "Abstract Background Parkinson’s disease (PD) is a neurodegenerative disorder characterized by a loss of dopaminergic neurons (DN) in the substantia nigra (SN). Several lines of evidence suggest that apoptotic cell death of DN is driven in part by non-cell autonomous mechanisms orchestrated by microglial cell-mediated inflammatory processes. Although the mechanisms and molecular network underlying this deleterious cross-talk between DN and microglial cells remain largely unknown, previous work indicates that, upon DN injury, activation of the β2 integrin subunit CD11b is required for microglia-mediated DN cell death. Interestingly, during brain development, the CD11b integrin is also involved in microglial induction of neuronal apoptosis and has been shown to act in concert with the DAP12 immunoreceptor. Whether such a developmental CD11b/DAP12 pathway could be reactivated in a pathological context such as PD and play a role in microglia-induced DN cell death is a tantalizing hypothesis that we wished to test in this study. Methods To test the possibility that DAP12 could be involved in microglia-associated DN injury, we used both in vitro and in vivo toxin-based experimental models of PD recapitulating microglial-mediated non-cell autonomous mechanisms of DN cell death. In vitro , enriched mesencephalic neuronal/microglial co-cultures were exposed to the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium (MPP+) whereas in vivo , mice were administrated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) according to acute or subchronic mode. Mice deficient for DAP12 or CD11b were used to determine the pathological function of the CD11b/DAP12 pathway in our disease models. Results Our results show that DAP12 and CD11b partially contribute to microglia-induced DN cell death in vitro . Yet, in vivo , mice deficient for either of these factors develop similar neuropathological alterations as their wild-type counterparts in two different MPTP mouse models of PD. Conclusion Overall, our data suggest that DAP12 and CD11b contribute to microglial-induced DN cell death in vitro but not in vivo in the MPTP mouse model of PD. Therefore, the CD11b/DAP12 pathway may not be considered as a promising therapeutic target for PD." @default.
• W2156165184 created "2016-06-24" @default.
• W2156165184 creator A5015803998 @default.
• W2156165184 creator A5025886288 @default.
• W2156165184 creator A5047802985 @default.
• W2156165184 creator A5065531665 @default.
• W2156165184 creator A5067769815 @default.
• W2156165184 creator A5069618227 @default.
• W2156165184 creator A5080760647 @default.
• W2156165184 date "2013-07-11" @default.
• W2156165184 modified "2023-09-27" @default.
• W2156165184 title "DAP12 and CD11b contribute to the microglial-induced death of dopaminergic neurons in vitro but not in vivo in the MPTP mouse model of Parkinson’s disease" @default.
• W2156165184 cites W1530199299 @default.
• W2156165184 cites W1595413626 @default.
• W2156165184 cites W1971701992 @default.
• W2156165184 cites W1979028882 @default.
• W2156165184 cites W2002148098 @default.
• W2156165184 cites W2008183439 @default.
• W2156165184 cites W2035908320 @default.
• W2156165184 cites W2036599150 @default.
• W2156165184 cites W2042393284 @default.
• W2156165184 cites W2051185006 @default.
• W2156165184 cites W2051940924 @default.
• W2156165184 cites W2057819734 @default.
• W2156165184 cites W2060061788 @default.
• W2156165184 cites W2079958878 @default.
• W2156165184 cites W2091836237 @default.
• W2156165184 cites W2103711259 @default.
• W2156165184 cites W2107865650 @default.
• W2156165184 cites W2111464898 @default.
• W2156165184 cites W2114813008 @default.
• W2156165184 cites W2130103159 @default.
• W2156165184 cites W2133084626 @default.
• W2156165184 cites W2133739669 @default.
• W2156165184 cites W2138227659 @default.
• W2156165184 cites W2167022467 @default.
• W2156165184 cites W2168221521 @default.
• W2156165184 cites W62603772 @default.
• W2156165184 doi "https://doi.org/10.1186/1742-2094-10-82" @default.
• W2156165184 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3720270" @default.
• W2156165184 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23844828" @default.
• W2156165184 hasPublicationYear "2013" @default.
• W2156165184 type Work @default.
• W2156165184 sameAs 2156165184 @default.
• W2156165184 citedByCount "11" @default.
• W2156165184 countsByYear W21561651842015 @default.
• W2156165184 countsByYear W21561651842017 @default.
• W2156165184 countsByYear W21561651842018 @default.
• W2156165184 countsByYear W21561651842019 @default.
• W2156165184 countsByYear W21561651842020 @default.
• W2156165184 countsByYear W21561651842021 @default.
• W2156165184 countsByYear W21561651842022 @default.
• W2156165184 countsByYear W21561651842023 @default.
• W2156165184 crossrefType "journal-article" @default.
• W2156165184 hasAuthorship W2156165184A5015803998 @default.
• W2156165184 hasAuthorship W2156165184A5025886288 @default.
• W2156165184 hasAuthorship W2156165184A5047802985 @default.
• W2156165184 hasAuthorship W2156165184A5065531665 @default.
• W2156165184 hasAuthorship W2156165184A5067769815 @default.
• W2156165184 hasAuthorship W2156165184A5069618227 @default.
• W2156165184 hasAuthorship W2156165184A5080760647 @default.
• W2156165184 hasBestOaLocation W21561651841 @default.
• W2156165184 hasConcept C137183658 @default.
• W2156165184 hasConcept C150903083 @default.
• W2156165184 hasConcept C169760540 @default.
• W2156165184 hasConcept C171779818 @default.
• W2156165184 hasConcept C190283241 @default.
• W2156165184 hasConcept C203014093 @default.
• W2156165184 hasConcept C207001950 @default.
• W2156165184 hasConcept C2776914184 @default.
• W2156165184 hasConcept C2778674702 @default.
• W2156165184 hasConcept C2779830541 @default.
• W2156165184 hasConcept C2780938664 @default.
• W2156165184 hasConcept C31573885 @default.
• W2156165184 hasConcept C513476851 @default.
• W2156165184 hasConcept C55493867 @default.
• W2156165184 hasConcept C86803240 @default.
• W2156165184 hasConcept C8891405 @default.
• W2156165184 hasConcept C95444343 @default.
• W2156165184 hasConceptScore W2156165184C137183658 @default.
• W2156165184 hasConceptScore W2156165184C150903083 @default.
• W2156165184 hasConceptScore W2156165184C169760540 @default.
• W2156165184 hasConceptScore W2156165184C171779818 @default.
• W2156165184 hasConceptScore W2156165184C190283241 @default.
• W2156165184 hasConceptScore W2156165184C203014093 @default.
• W2156165184 hasConceptScore W2156165184C207001950 @default.
• W2156165184 hasConceptScore W2156165184C2776914184 @default.
• W2156165184 hasConceptScore W2156165184C2778674702 @default.
• W2156165184 hasConceptScore W2156165184C2779830541 @default.
• W2156165184 hasConceptScore W2156165184C2780938664 @default.
• W2156165184 hasConceptScore W2156165184C31573885 @default.
• W2156165184 hasConceptScore W2156165184C513476851 @default.
• W2156165184 hasConceptScore W2156165184C55493867 @default.
• W2156165184 hasConceptScore W2156165184C86803240 @default.
• W2156165184 hasConceptScore W2156165184C8891405 @default.
• W2156165184 hasConceptScore W2156165184C95444343 @default.
• W2156165184 hasIssue "1" @default.
• W2156165184 hasLocation W21561651841 @default.
• W2156165184 hasLocation W21561651842 @default.
• W2156165184 hasLocation W21561651843 @default.

• next