Matches in SemOpenAlex for { <https://semopenalex.org/work/W2178857472> ?p ?o ?g. }
- W2178857472 endingPage "1664" @default.
- W2178857472 startingPage "1654" @default.
- W2178857472 abstract "OBJECT Hypoxia can induce cell death or trigger adaptive mechanisms to guarantee cell survival. Neuron-derived orphan receptor 1 (NOR-1) works as an early-response protein in response to a variety of environmental stresses. In this study, the authors evaluated the roles of NOR-1 in hypoxia-induced neuronal insults. METHODS Neuro-2a cells were exposed to oxygen/glucose deprivation (OGD). Cell viability, cell morphology, cas-pase-3 activity, DNA fragmentation, and cell apoptosis were assayed to determine the mechanisms of OGD-induced neuronal insults. RNA and protein analyses were carried out to evaluate the effects of OGD on expressions of NOR-1, cAMP response element-binding (CREB), and cellular inhibitor of apoptosis protein 2 (cIAP2) genes. Translations of these gene expressions were knocked down using RNA interference. Mice subjected to traumatic brain injury (TBI) and NOR-1 was immunodetected. RESULTS Exposure of neuro-2a cells to OGD decreased cell viability in a time-dependent manner. Additionally, OGD led to cell shrinkage, DNA fragmentation, and cell apoptosis. In parallel, treatment of neuro-2a cells with OGD time dependently increased cellular NOR-1 mRNA and protein expressions. Interestingly, administration of TBI also augmented NOR-1 levels in the impacted regions of mice. As to the mechanism, exposure to OGD increased nuclear levels of the transcription factor CREB protein. Downregulating CREB expression using RNA interference simultaneously inhibited OGD-induced NOR-1 mRNA expression. Also, levels of cIAP2 mRNA and protein in neuro-2a cells were augmented by OGD. After reducing cIAP2 translation, OGD-induced cell death was reduced. Sequentially, application of NOR-1 small interfering RNA to neuro-2a cells significantly inhibited OGD-induced cIAP2 mRNA expression and concurrently alleviated hypoxia-induced alterations in cell viability, caspase-3 activation, DNA damage, and cell apoptosis. CONCLUSIONS This study shows that NOR-1 can transduce survival signals in neuronal cells responsible for hypoxiainduced apoptotic insults through activation of a CREB/cIAP2-dependent mechanism." @default.
- W2178857472 created "2016-06-24" @default.
- W2178857472 creator A5008407911 @default.
- W2178857472 creator A5025014984 @default.
- W2178857472 creator A5025329742 @default.
- W2178857472 creator A5043969112 @default.
- W2178857472 creator A5064694317 @default.
- W2178857472 creator A5073525424 @default.
- W2178857472 creator A5076215944 @default.
- W2178857472 date "2016-06-01" @default.
- W2178857472 modified "2023-09-26" @default.
- W2178857472 title "Neuron-derived orphan receptor 1 transduces survival signals in neuronal cells in response to hypoxia-induced apoptotic insults" @default.
- W2178857472 cites W1589179621 @default.
- W2178857472 cites W1964156547 @default.
- W2178857472 cites W1964796194 @default.
- W2178857472 cites W1965147820 @default.
- W2178857472 cites W1969430540 @default.
- W2178857472 cites W1973589902 @default.
- W2178857472 cites W1983398917 @default.
- W2178857472 cites W1991090990 @default.
- W2178857472 cites W2000324336 @default.
- W2178857472 cites W2002400039 @default.
- W2178857472 cites W2004567612 @default.
- W2178857472 cites W2012382137 @default.
- W2178857472 cites W2021044488 @default.
- W2178857472 cites W2025897011 @default.
- W2178857472 cites W2036264929 @default.
- W2178857472 cites W2037728093 @default.
- W2178857472 cites W2047571097 @default.
- W2178857472 cites W2055145844 @default.
- W2178857472 cites W2058756209 @default.
- W2178857472 cites W2059756402 @default.
- W2178857472 cites W2060219934 @default.
- W2178857472 cites W2064804525 @default.
- W2178857472 cites W2065036369 @default.
- W2178857472 cites W2066779825 @default.
- W2178857472 cites W2084962044 @default.
- W2178857472 cites W2089397079 @default.
- W2178857472 cites W2089459615 @default.
- W2178857472 cites W2101803901 @default.
- W2178857472 cites W2102050957 @default.
- W2178857472 cites W2105362510 @default.
- W2178857472 cites W2121638241 @default.
- W2178857472 cites W2136212813 @default.
- W2178857472 cites W2144926889 @default.
- W2178857472 cites W2146780287 @default.
- W2178857472 cites W2156133860 @default.
- W2178857472 cites W2170159267 @default.
- W2178857472 cites W2319138051 @default.
- W2178857472 doi "https://doi.org/10.3171/2015.6.jns1535" @default.
- W2178857472 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26613168" @default.
- W2178857472 hasPublicationYear "2016" @default.
- W2178857472 type Work @default.
- W2178857472 sameAs 2178857472 @default.
- W2178857472 citedByCount "16" @default.
- W2178857472 countsByYear W21788574722017 @default.
- W2178857472 countsByYear W21788574722018 @default.
- W2178857472 countsByYear W21788574722019 @default.
- W2178857472 countsByYear W21788574722020 @default.
- W2178857472 countsByYear W21788574722021 @default.
- W2178857472 countsByYear W21788574722022 @default.
- W2178857472 crossrefType "journal-article" @default.
- W2178857472 hasAuthorship W2178857472A5008407911 @default.
- W2178857472 hasAuthorship W2178857472A5025014984 @default.
- W2178857472 hasAuthorship W2178857472A5025329742 @default.
- W2178857472 hasAuthorship W2178857472A5043969112 @default.
- W2178857472 hasAuthorship W2178857472A5064694317 @default.
- W2178857472 hasAuthorship W2178857472A5073525424 @default.
- W2178857472 hasAuthorship W2178857472A5076215944 @default.
- W2178857472 hasBestOaLocation W21788574721 @default.
- W2178857472 hasConcept C104317684 @default.
- W2178857472 hasConcept C105580179 @default.
- W2178857472 hasConcept C1491633281 @default.
- W2178857472 hasConcept C153911025 @default.
- W2178857472 hasConcept C1629964 @default.
- W2178857472 hasConcept C166703698 @default.
- W2178857472 hasConcept C190283241 @default.
- W2178857472 hasConcept C31573885 @default.
- W2178857472 hasConcept C43759708 @default.
- W2178857472 hasConcept C53227056 @default.
- W2178857472 hasConcept C55493867 @default.
- W2178857472 hasConcept C67705224 @default.
- W2178857472 hasConcept C86339819 @default.
- W2178857472 hasConcept C86803240 @default.
- W2178857472 hasConcept C95444343 @default.
- W2178857472 hasConceptScore W2178857472C104317684 @default.
- W2178857472 hasConceptScore W2178857472C105580179 @default.
- W2178857472 hasConceptScore W2178857472C1491633281 @default.
- W2178857472 hasConceptScore W2178857472C153911025 @default.
- W2178857472 hasConceptScore W2178857472C1629964 @default.
- W2178857472 hasConceptScore W2178857472C166703698 @default.
- W2178857472 hasConceptScore W2178857472C190283241 @default.
- W2178857472 hasConceptScore W2178857472C31573885 @default.
- W2178857472 hasConceptScore W2178857472C43759708 @default.
- W2178857472 hasConceptScore W2178857472C53227056 @default.
- W2178857472 hasConceptScore W2178857472C55493867 @default.
- W2178857472 hasConceptScore W2178857472C67705224 @default.
- W2178857472 hasConceptScore W2178857472C86339819 @default.