Intercommunications between brain capillary endothelial cells and glial cells increase the transcellular permeability of the blood–brain barrier during ischaemia
Increased cerebrovascular permeability is an important factor in the development of cerebral oedema after stroke, implicating the blood–brain barrier (BBB). To investigate the effect of hypoxia on the permeability changes, we used a cell culture model of the BBB consisting of a co-culture of brain c...
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| Autor*in: |
Brillault, Julien [verfasserIn] Berezowski, Vincent [verfasserIn] Cecchelli, Roméo [verfasserIn] |
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E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2002 |
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Online-Ressource |
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2002 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 83(2002), 4, Seite 0 |
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volume:83 ; year:2002 ; number:4 ; pages:0 |
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| DOI / URN: |
10.1046/j.1471-4159.2002.01186.x |
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| 520 | |a Increased cerebrovascular permeability is an important factor in the development of cerebral oedema after stroke, implicating the blood–brain barrier (BBB). To investigate the effect of hypoxia on the permeability changes, we used a cell culture model of the BBB consisting of a co-culture of brain capillary endothelial cells and glial cells. When endothelial cells from this co-culture model were submitted alone to hypoxic conditions, long exposures (48 h) were necessary to result in an increase in endothelial cell monolayer permeability to [3H]inulin. When endothelial cells were incubated in presence of glial cells, a huge increase in permeability occurred after 9 h of hypoxic conditions. Oxygen glucose deprivation (OGD) resulted in a much shorter time (i.e. 2 h) required for an increase in permeability. We have demonstrated that this OGD-induced permeability increase involves a transcellular rather than a paracellular pathway. Conditioned medium experiments showed that glial cells secrete soluble permeability factors during OGD. However, endothelial cells have to be made sensitive by OGD in order to respond to these glial soluble factors. This work shows that an early cross-talk between glial and endothelial cells occurs during ischaemic stroke and alters BBB transcellular transport by means of glial factor secretions. | ||
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10.1046/j.1471-4159.2002.01186.x doi (DE-627)NLEJ243134630 DE-627 ger DE-627 rakwb Brillault, Julien verfasserin aut Intercommunications between brain capillary endothelial cells and glial cells increase the transcellular permeability of the blood–brain barrier during ischaemia Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Increased cerebrovascular permeability is an important factor in the development of cerebral oedema after stroke, implicating the blood–brain barrier (BBB). To investigate the effect of hypoxia on the permeability changes, we used a cell culture model of the BBB consisting of a co-culture of brain capillary endothelial cells and glial cells. When endothelial cells from this co-culture model were submitted alone to hypoxic conditions, long exposures (48 h) were necessary to result in an increase in endothelial cell monolayer permeability to [3H]inulin. When endothelial cells were incubated in presence of glial cells, a huge increase in permeability occurred after 9 h of hypoxic conditions. Oxygen glucose deprivation (OGD) resulted in a much shorter time (i.e. 2 h) required for an increase in permeability. We have demonstrated that this OGD-induced permeability increase involves a transcellular rather than a paracellular pathway. Conditioned medium experiments showed that glial cells secrete soluble permeability factors during OGD. However, endothelial cells have to be made sensitive by OGD in order to respond to these glial soluble factors. This work shows that an early cross-talk between glial and endothelial cells occurs during ischaemic stroke and alters BBB transcellular transport by means of glial factor secretions. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| blood–brain barrier Berezowski, Vincent verfasserin aut Cecchelli, Roméo verfasserin aut Dehouck, Marie-Pierre oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 83(2002), 4, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:83 year:2002 number:4 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2002.01186.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 83 2002 4 0 |
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10.1046/j.1471-4159.2002.01186.x doi (DE-627)NLEJ243134630 DE-627 ger DE-627 rakwb Brillault, Julien verfasserin aut Intercommunications between brain capillary endothelial cells and glial cells increase the transcellular permeability of the blood–brain barrier during ischaemia Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Increased cerebrovascular permeability is an important factor in the development of cerebral oedema after stroke, implicating the blood–brain barrier (BBB). To investigate the effect of hypoxia on the permeability changes, we used a cell culture model of the BBB consisting of a co-culture of brain capillary endothelial cells and glial cells. When endothelial cells from this co-culture model were submitted alone to hypoxic conditions, long exposures (48 h) were necessary to result in an increase in endothelial cell monolayer permeability to [3H]inulin. When endothelial cells were incubated in presence of glial cells, a huge increase in permeability occurred after 9 h of hypoxic conditions. Oxygen glucose deprivation (OGD) resulted in a much shorter time (i.e. 2 h) required for an increase in permeability. We have demonstrated that this OGD-induced permeability increase involves a transcellular rather than a paracellular pathway. Conditioned medium experiments showed that glial cells secrete soluble permeability factors during OGD. However, endothelial cells have to be made sensitive by OGD in order to respond to these glial soluble factors. This work shows that an early cross-talk between glial and endothelial cells occurs during ischaemic stroke and alters BBB transcellular transport by means of glial factor secretions. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| blood–brain barrier Berezowski, Vincent verfasserin aut Cecchelli, Roméo verfasserin aut Dehouck, Marie-Pierre oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 83(2002), 4, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:83 year:2002 number:4 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2002.01186.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 83 2002 4 0 |
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10.1046/j.1471-4159.2002.01186.x doi (DE-627)NLEJ243134630 DE-627 ger DE-627 rakwb Brillault, Julien verfasserin aut Intercommunications between brain capillary endothelial cells and glial cells increase the transcellular permeability of the blood–brain barrier during ischaemia Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Increased cerebrovascular permeability is an important factor in the development of cerebral oedema after stroke, implicating the blood–brain barrier (BBB). To investigate the effect of hypoxia on the permeability changes, we used a cell culture model of the BBB consisting of a co-culture of brain capillary endothelial cells and glial cells. When endothelial cells from this co-culture model were submitted alone to hypoxic conditions, long exposures (48 h) were necessary to result in an increase in endothelial cell monolayer permeability to [3H]inulin. When endothelial cells were incubated in presence of glial cells, a huge increase in permeability occurred after 9 h of hypoxic conditions. Oxygen glucose deprivation (OGD) resulted in a much shorter time (i.e. 2 h) required for an increase in permeability. We have demonstrated that this OGD-induced permeability increase involves a transcellular rather than a paracellular pathway. Conditioned medium experiments showed that glial cells secrete soluble permeability factors during OGD. However, endothelial cells have to be made sensitive by OGD in order to respond to these glial soluble factors. This work shows that an early cross-talk between glial and endothelial cells occurs during ischaemic stroke and alters BBB transcellular transport by means of glial factor secretions. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| blood–brain barrier Berezowski, Vincent verfasserin aut Cecchelli, Roméo verfasserin aut Dehouck, Marie-Pierre oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 83(2002), 4, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:83 year:2002 number:4 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2002.01186.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 83 2002 4 0 |
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10.1046/j.1471-4159.2002.01186.x doi (DE-627)NLEJ243134630 DE-627 ger DE-627 rakwb Brillault, Julien verfasserin aut Intercommunications between brain capillary endothelial cells and glial cells increase the transcellular permeability of the blood–brain barrier during ischaemia Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Increased cerebrovascular permeability is an important factor in the development of cerebral oedema after stroke, implicating the blood–brain barrier (BBB). To investigate the effect of hypoxia on the permeability changes, we used a cell culture model of the BBB consisting of a co-culture of brain capillary endothelial cells and glial cells. When endothelial cells from this co-culture model were submitted alone to hypoxic conditions, long exposures (48 h) were necessary to result in an increase in endothelial cell monolayer permeability to [3H]inulin. When endothelial cells were incubated in presence of glial cells, a huge increase in permeability occurred after 9 h of hypoxic conditions. Oxygen glucose deprivation (OGD) resulted in a much shorter time (i.e. 2 h) required for an increase in permeability. We have demonstrated that this OGD-induced permeability increase involves a transcellular rather than a paracellular pathway. Conditioned medium experiments showed that glial cells secrete soluble permeability factors during OGD. However, endothelial cells have to be made sensitive by OGD in order to respond to these glial soluble factors. This work shows that an early cross-talk between glial and endothelial cells occurs during ischaemic stroke and alters BBB transcellular transport by means of glial factor secretions. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| blood–brain barrier Berezowski, Vincent verfasserin aut Cecchelli, Roméo verfasserin aut Dehouck, Marie-Pierre oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 83(2002), 4, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:83 year:2002 number:4 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2002.01186.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 83 2002 4 0 |
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10.1046/j.1471-4159.2002.01186.x doi (DE-627)NLEJ243134630 DE-627 ger DE-627 rakwb Brillault, Julien verfasserin aut Intercommunications between brain capillary endothelial cells and glial cells increase the transcellular permeability of the blood–brain barrier during ischaemia Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Increased cerebrovascular permeability is an important factor in the development of cerebral oedema after stroke, implicating the blood–brain barrier (BBB). To investigate the effect of hypoxia on the permeability changes, we used a cell culture model of the BBB consisting of a co-culture of brain capillary endothelial cells and glial cells. When endothelial cells from this co-culture model were submitted alone to hypoxic conditions, long exposures (48 h) were necessary to result in an increase in endothelial cell monolayer permeability to [3H]inulin. When endothelial cells were incubated in presence of glial cells, a huge increase in permeability occurred after 9 h of hypoxic conditions. Oxygen glucose deprivation (OGD) resulted in a much shorter time (i.e. 2 h) required for an increase in permeability. We have demonstrated that this OGD-induced permeability increase involves a transcellular rather than a paracellular pathway. Conditioned medium experiments showed that glial cells secrete soluble permeability factors during OGD. However, endothelial cells have to be made sensitive by OGD in order to respond to these glial soluble factors. This work shows that an early cross-talk between glial and endothelial cells occurs during ischaemic stroke and alters BBB transcellular transport by means of glial factor secretions. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| blood–brain barrier Berezowski, Vincent verfasserin aut Cecchelli, Roméo verfasserin aut Dehouck, Marie-Pierre oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 83(2002), 4, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:83 year:2002 number:4 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2002.01186.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 83 2002 4 0 |
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Intercommunications between brain capillary endothelial cells and glial cells increase the transcellular permeability of the blood–brain barrier during ischaemia |
| abstract |
Increased cerebrovascular permeability is an important factor in the development of cerebral oedema after stroke, implicating the blood–brain barrier (BBB). To investigate the effect of hypoxia on the permeability changes, we used a cell culture model of the BBB consisting of a co-culture of brain capillary endothelial cells and glial cells. When endothelial cells from this co-culture model were submitted alone to hypoxic conditions, long exposures (48 h) were necessary to result in an increase in endothelial cell monolayer permeability to [3H]inulin. When endothelial cells were incubated in presence of glial cells, a huge increase in permeability occurred after 9 h of hypoxic conditions. Oxygen glucose deprivation (OGD) resulted in a much shorter time (i.e. 2 h) required for an increase in permeability. We have demonstrated that this OGD-induced permeability increase involves a transcellular rather than a paracellular pathway. Conditioned medium experiments showed that glial cells secrete soluble permeability factors during OGD. However, endothelial cells have to be made sensitive by OGD in order to respond to these glial soluble factors. This work shows that an early cross-talk between glial and endothelial cells occurs during ischaemic stroke and alters BBB transcellular transport by means of glial factor secretions. |
| abstractGer |
Increased cerebrovascular permeability is an important factor in the development of cerebral oedema after stroke, implicating the blood–brain barrier (BBB). To investigate the effect of hypoxia on the permeability changes, we used a cell culture model of the BBB consisting of a co-culture of brain capillary endothelial cells and glial cells. When endothelial cells from this co-culture model were submitted alone to hypoxic conditions, long exposures (48 h) were necessary to result in an increase in endothelial cell monolayer permeability to [3H]inulin. When endothelial cells were incubated in presence of glial cells, a huge increase in permeability occurred after 9 h of hypoxic conditions. Oxygen glucose deprivation (OGD) resulted in a much shorter time (i.e. 2 h) required for an increase in permeability. We have demonstrated that this OGD-induced permeability increase involves a transcellular rather than a paracellular pathway. Conditioned medium experiments showed that glial cells secrete soluble permeability factors during OGD. However, endothelial cells have to be made sensitive by OGD in order to respond to these glial soluble factors. This work shows that an early cross-talk between glial and endothelial cells occurs during ischaemic stroke and alters BBB transcellular transport by means of glial factor secretions. |
| abstract_unstemmed |
Increased cerebrovascular permeability is an important factor in the development of cerebral oedema after stroke, implicating the blood–brain barrier (BBB). To investigate the effect of hypoxia on the permeability changes, we used a cell culture model of the BBB consisting of a co-culture of brain capillary endothelial cells and glial cells. When endothelial cells from this co-culture model were submitted alone to hypoxic conditions, long exposures (48 h) were necessary to result in an increase in endothelial cell monolayer permeability to [3H]inulin. When endothelial cells were incubated in presence of glial cells, a huge increase in permeability occurred after 9 h of hypoxic conditions. Oxygen glucose deprivation (OGD) resulted in a much shorter time (i.e. 2 h) required for an increase in permeability. We have demonstrated that this OGD-induced permeability increase involves a transcellular rather than a paracellular pathway. Conditioned medium experiments showed that glial cells secrete soluble permeability factors during OGD. However, endothelial cells have to be made sensitive by OGD in order to respond to these glial soluble factors. This work shows that an early cross-talk between glial and endothelial cells occurs during ischaemic stroke and alters BBB transcellular transport by means of glial factor secretions. |
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Intercommunications between brain capillary endothelial cells and glial cells increase the transcellular permeability of the blood–brain barrier during ischaemia |
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Berezowski, Vincent Cecchelli, Roméo Dehouck, Marie-Pierre |
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10.1046/j.1471-4159.2002.01186.x |
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