Delayed genomic responses to transient middle cerebral artery occlusion in the rat
Ischemic stress in the brain induces acute and massive neuronal death in the targeted area, which is followed by a second round of detrimental processes, called delayed neuronal death, in the neighboring areas. To test the hypothesis that transcriptional control plays a role in the pathophysiology o...
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| Autor*in: |
Kim, Jung-Bin [verfasserIn] Piao, Chun-Shu [verfasserIn] Lee, Kang Woo [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2004 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2004 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 89(2004), 5, Seite 0 |
| Übergeordnetes Werk: |
volume:89 ; year:2004 ; number:5 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1111/j.1471-4159.2004.02429.x |
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| 520 | |a Ischemic stress in the brain induces acute and massive neuronal death in the targeted area, which is followed by a second round of detrimental processes, called delayed neuronal death, in the neighboring areas. To test the hypothesis that transcriptional control plays a role in the pathophysiology of the postischemic brain, the genomic responses that occurred in the brain at 3, 6 and, 12 h, and 1, 2 or 4 days after transient middle cerebral artery occlusion (MCAO) were examined using a microarray harboring 5000 rat cDNAs. This analysis indicated that the number of up-regulated genes was gradually increased, along with the concomitant reduction in the number of down-regulated genes, until 12 h to 1 day after MCAO. It was followed by a delayed surge of down-regulated genes at 2 days after MCAO. Northern blots and immunohistological analysis confirmed the validity of these microarray data. We present a list of 85 genes that were up-regulated more than 2.3-fold between 12 h and 4 days after MCAO, which included 56 novel genes whose expression has not previously been implicated in ischemic pathophysiology. The list included genes involved in oxidative stress, inflammation, extracellular matrix (ECM), neuronal development and differentiation processes. Together these results suggest that the pathophysiology of the postischemic brain proceeds by the transcriptional activation of genes related to the process of delayed neuronal damage and/or recovery and repair. | ||
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10.1111/j.1471-4159.2004.02429.x doi (DE-627)NLEJ243121849 DE-627 ger DE-627 rakwb Kim, Jung-Bin verfasserin aut Delayed genomic responses to transient middle cerebral artery occlusion in the rat Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Ischemic stress in the brain induces acute and massive neuronal death in the targeted area, which is followed by a second round of detrimental processes, called delayed neuronal death, in the neighboring areas. To test the hypothesis that transcriptional control plays a role in the pathophysiology of the postischemic brain, the genomic responses that occurred in the brain at 3, 6 and, 12 h, and 1, 2 or 4 days after transient middle cerebral artery occlusion (MCAO) were examined using a microarray harboring 5000 rat cDNAs. This analysis indicated that the number of up-regulated genes was gradually increased, along with the concomitant reduction in the number of down-regulated genes, until 12 h to 1 day after MCAO. It was followed by a delayed surge of down-regulated genes at 2 days after MCAO. Northern blots and immunohistological analysis confirmed the validity of these microarray data. We present a list of 85 genes that were up-regulated more than 2.3-fold between 12 h and 4 days after MCAO, which included 56 novel genes whose expression has not previously been implicated in ischemic pathophysiology. The list included genes involved in oxidative stress, inflammation, extracellular matrix (ECM), neuronal development and differentiation processes. Together these results suggest that the pathophysiology of the postischemic brain proceeds by the transcriptional activation of genes related to the process of delayed neuronal damage and/or recovery and repair. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| delayed neuronal death Piao, Chun-Shu verfasserin aut Lee, Kang Woo verfasserin aut Han, Pyung-Lim oth Ahn, Joon Ik oth Lee, Yong Sung oth Lee, Ja-Kyeong oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 89(2004), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:89 year:2004 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.2004.02429.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 89 2004 5 0 |
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10.1111/j.1471-4159.2004.02429.x doi (DE-627)NLEJ243121849 DE-627 ger DE-627 rakwb Kim, Jung-Bin verfasserin aut Delayed genomic responses to transient middle cerebral artery occlusion in the rat Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Ischemic stress in the brain induces acute and massive neuronal death in the targeted area, which is followed by a second round of detrimental processes, called delayed neuronal death, in the neighboring areas. To test the hypothesis that transcriptional control plays a role in the pathophysiology of the postischemic brain, the genomic responses that occurred in the brain at 3, 6 and, 12 h, and 1, 2 or 4 days after transient middle cerebral artery occlusion (MCAO) were examined using a microarray harboring 5000 rat cDNAs. This analysis indicated that the number of up-regulated genes was gradually increased, along with the concomitant reduction in the number of down-regulated genes, until 12 h to 1 day after MCAO. It was followed by a delayed surge of down-regulated genes at 2 days after MCAO. Northern blots and immunohistological analysis confirmed the validity of these microarray data. We present a list of 85 genes that were up-regulated more than 2.3-fold between 12 h and 4 days after MCAO, which included 56 novel genes whose expression has not previously been implicated in ischemic pathophysiology. The list included genes involved in oxidative stress, inflammation, extracellular matrix (ECM), neuronal development and differentiation processes. Together these results suggest that the pathophysiology of the postischemic brain proceeds by the transcriptional activation of genes related to the process of delayed neuronal damage and/or recovery and repair. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| delayed neuronal death Piao, Chun-Shu verfasserin aut Lee, Kang Woo verfasserin aut Han, Pyung-Lim oth Ahn, Joon Ik oth Lee, Yong Sung oth Lee, Ja-Kyeong oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 89(2004), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:89 year:2004 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.2004.02429.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 89 2004 5 0 |
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10.1111/j.1471-4159.2004.02429.x doi (DE-627)NLEJ243121849 DE-627 ger DE-627 rakwb Kim, Jung-Bin verfasserin aut Delayed genomic responses to transient middle cerebral artery occlusion in the rat Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Ischemic stress in the brain induces acute and massive neuronal death in the targeted area, which is followed by a second round of detrimental processes, called delayed neuronal death, in the neighboring areas. To test the hypothesis that transcriptional control plays a role in the pathophysiology of the postischemic brain, the genomic responses that occurred in the brain at 3, 6 and, 12 h, and 1, 2 or 4 days after transient middle cerebral artery occlusion (MCAO) were examined using a microarray harboring 5000 rat cDNAs. This analysis indicated that the number of up-regulated genes was gradually increased, along with the concomitant reduction in the number of down-regulated genes, until 12 h to 1 day after MCAO. It was followed by a delayed surge of down-regulated genes at 2 days after MCAO. Northern blots and immunohistological analysis confirmed the validity of these microarray data. We present a list of 85 genes that were up-regulated more than 2.3-fold between 12 h and 4 days after MCAO, which included 56 novel genes whose expression has not previously been implicated in ischemic pathophysiology. The list included genes involved in oxidative stress, inflammation, extracellular matrix (ECM), neuronal development and differentiation processes. Together these results suggest that the pathophysiology of the postischemic brain proceeds by the transcriptional activation of genes related to the process of delayed neuronal damage and/or recovery and repair. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| delayed neuronal death Piao, Chun-Shu verfasserin aut Lee, Kang Woo verfasserin aut Han, Pyung-Lim oth Ahn, Joon Ik oth Lee, Yong Sung oth Lee, Ja-Kyeong oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 89(2004), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:89 year:2004 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.2004.02429.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 89 2004 5 0 |
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10.1111/j.1471-4159.2004.02429.x doi (DE-627)NLEJ243121849 DE-627 ger DE-627 rakwb Kim, Jung-Bin verfasserin aut Delayed genomic responses to transient middle cerebral artery occlusion in the rat Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Ischemic stress in the brain induces acute and massive neuronal death in the targeted area, which is followed by a second round of detrimental processes, called delayed neuronal death, in the neighboring areas. To test the hypothesis that transcriptional control plays a role in the pathophysiology of the postischemic brain, the genomic responses that occurred in the brain at 3, 6 and, 12 h, and 1, 2 or 4 days after transient middle cerebral artery occlusion (MCAO) were examined using a microarray harboring 5000 rat cDNAs. This analysis indicated that the number of up-regulated genes was gradually increased, along with the concomitant reduction in the number of down-regulated genes, until 12 h to 1 day after MCAO. It was followed by a delayed surge of down-regulated genes at 2 days after MCAO. Northern blots and immunohistological analysis confirmed the validity of these microarray data. We present a list of 85 genes that were up-regulated more than 2.3-fold between 12 h and 4 days after MCAO, which included 56 novel genes whose expression has not previously been implicated in ischemic pathophysiology. The list included genes involved in oxidative stress, inflammation, extracellular matrix (ECM), neuronal development and differentiation processes. Together these results suggest that the pathophysiology of the postischemic brain proceeds by the transcriptional activation of genes related to the process of delayed neuronal damage and/or recovery and repair. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| delayed neuronal death Piao, Chun-Shu verfasserin aut Lee, Kang Woo verfasserin aut Han, Pyung-Lim oth Ahn, Joon Ik oth Lee, Yong Sung oth Lee, Ja-Kyeong oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 89(2004), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:89 year:2004 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.2004.02429.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 89 2004 5 0 |
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10.1111/j.1471-4159.2004.02429.x doi (DE-627)NLEJ243121849 DE-627 ger DE-627 rakwb Kim, Jung-Bin verfasserin aut Delayed genomic responses to transient middle cerebral artery occlusion in the rat Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Ischemic stress in the brain induces acute and massive neuronal death in the targeted area, which is followed by a second round of detrimental processes, called delayed neuronal death, in the neighboring areas. To test the hypothesis that transcriptional control plays a role in the pathophysiology of the postischemic brain, the genomic responses that occurred in the brain at 3, 6 and, 12 h, and 1, 2 or 4 days after transient middle cerebral artery occlusion (MCAO) were examined using a microarray harboring 5000 rat cDNAs. This analysis indicated that the number of up-regulated genes was gradually increased, along with the concomitant reduction in the number of down-regulated genes, until 12 h to 1 day after MCAO. It was followed by a delayed surge of down-regulated genes at 2 days after MCAO. Northern blots and immunohistological analysis confirmed the validity of these microarray data. We present a list of 85 genes that were up-regulated more than 2.3-fold between 12 h and 4 days after MCAO, which included 56 novel genes whose expression has not previously been implicated in ischemic pathophysiology. The list included genes involved in oxidative stress, inflammation, extracellular matrix (ECM), neuronal development and differentiation processes. Together these results suggest that the pathophysiology of the postischemic brain proceeds by the transcriptional activation of genes related to the process of delayed neuronal damage and/or recovery and repair. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| delayed neuronal death Piao, Chun-Shu verfasserin aut Lee, Kang Woo verfasserin aut Han, Pyung-Lim oth Ahn, Joon Ik oth Lee, Yong Sung oth Lee, Ja-Kyeong oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 89(2004), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:89 year:2004 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.2004.02429.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 89 2004 5 0 |
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Delayed genomic responses to transient middle cerebral artery occlusion in the rat |
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Ischemic stress in the brain induces acute and massive neuronal death in the targeted area, which is followed by a second round of detrimental processes, called delayed neuronal death, in the neighboring areas. To test the hypothesis that transcriptional control plays a role in the pathophysiology of the postischemic brain, the genomic responses that occurred in the brain at 3, 6 and, 12 h, and 1, 2 or 4 days after transient middle cerebral artery occlusion (MCAO) were examined using a microarray harboring 5000 rat cDNAs. This analysis indicated that the number of up-regulated genes was gradually increased, along with the concomitant reduction in the number of down-regulated genes, until 12 h to 1 day after MCAO. It was followed by a delayed surge of down-regulated genes at 2 days after MCAO. Northern blots and immunohistological analysis confirmed the validity of these microarray data. We present a list of 85 genes that were up-regulated more than 2.3-fold between 12 h and 4 days after MCAO, which included 56 novel genes whose expression has not previously been implicated in ischemic pathophysiology. The list included genes involved in oxidative stress, inflammation, extracellular matrix (ECM), neuronal development and differentiation processes. Together these results suggest that the pathophysiology of the postischemic brain proceeds by the transcriptional activation of genes related to the process of delayed neuronal damage and/or recovery and repair. |
| abstractGer |
Ischemic stress in the brain induces acute and massive neuronal death in the targeted area, which is followed by a second round of detrimental processes, called delayed neuronal death, in the neighboring areas. To test the hypothesis that transcriptional control plays a role in the pathophysiology of the postischemic brain, the genomic responses that occurred in the brain at 3, 6 and, 12 h, and 1, 2 or 4 days after transient middle cerebral artery occlusion (MCAO) were examined using a microarray harboring 5000 rat cDNAs. This analysis indicated that the number of up-regulated genes was gradually increased, along with the concomitant reduction in the number of down-regulated genes, until 12 h to 1 day after MCAO. It was followed by a delayed surge of down-regulated genes at 2 days after MCAO. Northern blots and immunohistological analysis confirmed the validity of these microarray data. We present a list of 85 genes that were up-regulated more than 2.3-fold between 12 h and 4 days after MCAO, which included 56 novel genes whose expression has not previously been implicated in ischemic pathophysiology. The list included genes involved in oxidative stress, inflammation, extracellular matrix (ECM), neuronal development and differentiation processes. Together these results suggest that the pathophysiology of the postischemic brain proceeds by the transcriptional activation of genes related to the process of delayed neuronal damage and/or recovery and repair. |
| abstract_unstemmed |
Ischemic stress in the brain induces acute and massive neuronal death in the targeted area, which is followed by a second round of detrimental processes, called delayed neuronal death, in the neighboring areas. To test the hypothesis that transcriptional control plays a role in the pathophysiology of the postischemic brain, the genomic responses that occurred in the brain at 3, 6 and, 12 h, and 1, 2 or 4 days after transient middle cerebral artery occlusion (MCAO) were examined using a microarray harboring 5000 rat cDNAs. This analysis indicated that the number of up-regulated genes was gradually increased, along with the concomitant reduction in the number of down-regulated genes, until 12 h to 1 day after MCAO. It was followed by a delayed surge of down-regulated genes at 2 days after MCAO. Northern blots and immunohistological analysis confirmed the validity of these microarray data. We present a list of 85 genes that were up-regulated more than 2.3-fold between 12 h and 4 days after MCAO, which included 56 novel genes whose expression has not previously been implicated in ischemic pathophysiology. The list included genes involved in oxidative stress, inflammation, extracellular matrix (ECM), neuronal development and differentiation processes. Together these results suggest that the pathophysiology of the postischemic brain proceeds by the transcriptional activation of genes related to the process of delayed neuronal damage and/or recovery and repair. |
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Delayed genomic responses to transient middle cerebral artery occlusion in the rat |
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Piao, Chun-Shu Lee, Kang Woo Han, Pyung-Lim Ahn, Joon Ik Lee, Yong Sung Lee, Ja-Kyeong |
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