BID mediates oxygen-glucose deprivation-induced neuronal injury in organotypic hippocampal slice cultures and modulates tissue inflammation in a transient focal cerebral ischemia model without changing lesion volu
The BH3 interacting-domain death agonist (BID) is a pro-apoptotic protein involved in death receptor-induced and mitochondria-mediated apoptosis. Recently, it has also been suggested that BID is involved in the regulation of inflammatory responses in the central nervous system. We found that BID def...
| Main Authors: | , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2016-02-01
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| Series: | Frontiers in Cellular Neuroscience |
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| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fncel.2016.00014/full |
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| author | Nellie Anne Martin Helena eBonner Maria Louise Elkjær Beatrice eD'Orsi Gang eChen Hans-Georg eKönig Martina eSvensson Tomas eDeierborg Shona ePfeiffer Jochen H.M. Prehn Kate Lykke Lambertsen |
| author_facet | Nellie Anne Martin Helena eBonner Maria Louise Elkjær Beatrice eD'Orsi Gang eChen Hans-Georg eKönig Martina eSvensson Tomas eDeierborg Shona ePfeiffer Jochen H.M. Prehn Kate Lykke Lambertsen |
| author_sort | Nellie Anne Martin |
| collection | DOAJ |
| description | The BH3 interacting-domain death agonist (BID) is a pro-apoptotic protein involved in death receptor-induced and mitochondria-mediated apoptosis. Recently, it has also been suggested that BID is involved in the regulation of inflammatory responses in the central nervous system. We found that BID deficiency protected organotypic hippocampal slice cultures in vitro from neuronal injury induced by oxygen-glucose deprivation. In vivo, BID-knockout (KO) mice and WT mice were subjected to 60 minutes of transient middle cerebral artery occlusion to induce focal cerebral ischemia, and allowed to recover for 24 hours. Infarct volumes and functional outcome were assessed and the inflammatory response was evaluated using immunofluorescence, Western blotting, quantitative PCR and Mesoscale multiplex analysis. We observed no difference in the infarct volume or neurological outcome between BID-KO and WT mice. The inflammatory response was reduced by BID deficiency as indicated by a change in microglial/leukocyte response. In conclusion, our data suggest that BID deficiency is neuroprotective in an in vitro model and modulates the inflammatory response to focal cerebral ischemia in vivo. However, this is not translated into a robust neuroprotection in vivo. |
| first_indexed | 2024-12-16T17:52:18Z |
| format | Article |
| id | doaj.art-b8fc2f40be5b41e3b9494c0393ba8895 |
| institution | Directory Open Access Journal |
| issn | 1662-5102 |
| language | English |
| last_indexed | 2024-12-16T17:52:18Z |
| publishDate | 2016-02-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cellular Neuroscience |
| spelling | doaj.art-b8fc2f40be5b41e3b9494c0393ba88952022-12-21T22:22:16ZengFrontiers Media S.A.Frontiers in Cellular Neuroscience1662-51022016-02-011010.3389/fncel.2016.00014172171BID mediates oxygen-glucose deprivation-induced neuronal injury in organotypic hippocampal slice cultures and modulates tissue inflammation in a transient focal cerebral ischemia model without changing lesion voluNellie Anne Martin0Helena eBonner1Maria Louise Elkjær2Beatrice eD'Orsi3Gang eChen4Hans-Georg eKönig5Martina eSvensson6Tomas eDeierborg7Shona ePfeiffer8Jochen H.M. Prehn9Kate Lykke Lambertsen10University of Southern DenmarkRoyal College of Surgeons in IrelandUniversity of Southern DenmarkRoyal College of Surgeons in IrelandRoyal College of Surgeons in IrelandRoyal College of Surgeons in IrelandLund UniversityLund UniversityRoyal College of Surgeons in IrelandRoyal College of Surgeons in IrelandUniversity of Southern DenmarkThe BH3 interacting-domain death agonist (BID) is a pro-apoptotic protein involved in death receptor-induced and mitochondria-mediated apoptosis. Recently, it has also been suggested that BID is involved in the regulation of inflammatory responses in the central nervous system. We found that BID deficiency protected organotypic hippocampal slice cultures in vitro from neuronal injury induced by oxygen-glucose deprivation. In vivo, BID-knockout (KO) mice and WT mice were subjected to 60 minutes of transient middle cerebral artery occlusion to induce focal cerebral ischemia, and allowed to recover for 24 hours. Infarct volumes and functional outcome were assessed and the inflammatory response was evaluated using immunofluorescence, Western blotting, quantitative PCR and Mesoscale multiplex analysis. We observed no difference in the infarct volume or neurological outcome between BID-KO and WT mice. The inflammatory response was reduced by BID deficiency as indicated by a change in microglial/leukocyte response. In conclusion, our data suggest that BID deficiency is neuroprotective in an in vitro model and modulates the inflammatory response to focal cerebral ischemia in vivo. However, this is not translated into a robust neuroprotection in vivo.http://journal.frontiersin.org/Journal/10.3389/fncel.2016.00014/fullInflammationBIDfocal cerebral ischemianeuronal injuryOrganotypic hippocampal slice cultures |
| spellingShingle | Nellie Anne Martin Helena eBonner Maria Louise Elkjær Beatrice eD'Orsi Gang eChen Hans-Georg eKönig Martina eSvensson Tomas eDeierborg Shona ePfeiffer Jochen H.M. Prehn Kate Lykke Lambertsen BID mediates oxygen-glucose deprivation-induced neuronal injury in organotypic hippocampal slice cultures and modulates tissue inflammation in a transient focal cerebral ischemia model without changing lesion volu Frontiers in Cellular Neuroscience Inflammation BID focal cerebral ischemia neuronal injury Organotypic hippocampal slice cultures |
| title | BID mediates oxygen-glucose deprivation-induced neuronal injury in organotypic hippocampal slice cultures and modulates tissue inflammation in a transient focal cerebral ischemia model without changing lesion volu |
| title_full | BID mediates oxygen-glucose deprivation-induced neuronal injury in organotypic hippocampal slice cultures and modulates tissue inflammation in a transient focal cerebral ischemia model without changing lesion volu |
| title_fullStr | BID mediates oxygen-glucose deprivation-induced neuronal injury in organotypic hippocampal slice cultures and modulates tissue inflammation in a transient focal cerebral ischemia model without changing lesion volu |
| title_full_unstemmed | BID mediates oxygen-glucose deprivation-induced neuronal injury in organotypic hippocampal slice cultures and modulates tissue inflammation in a transient focal cerebral ischemia model without changing lesion volu |
| title_short | BID mediates oxygen-glucose deprivation-induced neuronal injury in organotypic hippocampal slice cultures and modulates tissue inflammation in a transient focal cerebral ischemia model without changing lesion volu |
| title_sort | bid mediates oxygen glucose deprivation induced neuronal injury in organotypic hippocampal slice cultures and modulates tissue inflammation in a transient focal cerebral ischemia model without changing lesion volu |
| topic | Inflammation BID focal cerebral ischemia neuronal injury Organotypic hippocampal slice cultures |
| url | http://journal.frontiersin.org/Journal/10.3389/fncel.2016.00014/full |
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