Advanced

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 Volume.

Martin, Nellie Anne; Bonner, Helena; Elkjær, Maria Louise; D'Orsi, Beatrice; Chen, Gang; König, Hans Georg; Svensson, Martina LU ; Deierborg, Tomas LU ; Pfeiffer, Shona and Prehn, Jochen H, et al. (2016) In Frontiers in Cellular Neuroscience 10.
Abstract
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 wild type (WT) mice were subjected to 60 min of transient middle cerebral artery occlusion (tMCAO) to induce focal cerebral ischemia, and allowed to recover for 24 h. Infarct volumes and functional outcome were assessed and the inflammatory response was evaluated using... (More)
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 wild type (WT) mice were subjected to 60 min of transient middle cerebral artery occlusion (tMCAO) to induce focal cerebral ischemia, and allowed to recover for 24 h. Infarct volumes and functional outcome were assessed and the inflammatory response was evaluated using immunofluorescence, Western blotting, quantitative PCR (qPCR) 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. (Less)
Please use this url to cite or link to this publication:
author
, et al. (More)
(Less)
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Frontiers in Cellular Neuroscience
volume
10
publisher
Frontiers
external identifiers
  • pmid:26869884
  • scopus:84958750539
  • wos:000369141400002
ISSN
1662-5102
DOI
10.3389/fncel.2016.00014
language
English
LU publication?
yes
id
9ec318c5-7731-40ec-b2c9-00ec19ddf90c (old id 8825675)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/26869884?dopt=Abstract
date added to LUP
2016-03-04 11:19:00
date last changed
2017-09-24 04:11:43
@article{9ec318c5-7731-40ec-b2c9-00ec19ddf90c,
  abstract     = {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 wild type (WT) mice were subjected to 60 min of transient middle cerebral artery occlusion (tMCAO) to induce focal cerebral ischemia, and allowed to recover for 24 h. Infarct volumes and functional outcome were assessed and the inflammatory response was evaluated using immunofluorescence, Western blotting, quantitative PCR (qPCR) 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.},
  articleno    = {14},
  author       = {Martin, Nellie Anne and Bonner, Helena and Elkjær, Maria Louise and D'Orsi, Beatrice and Chen, Gang and König, Hans Georg and Svensson, Martina and Deierborg, Tomas and Pfeiffer, Shona and Prehn, Jochen H and Lambertsen, Kate Lykke},
  issn         = {1662-5102},
  language     = {eng},
  publisher    = {Frontiers},
  series       = {Frontiers in Cellular Neuroscience},
  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 Volume.},
  url          = {http://dx.doi.org/10.3389/fncel.2016.00014},
  volume       = {10},
  year         = {2016},
}