Cultured Astrocytes Release a Factor that Decreases Endothelin-1 Secretion by Brain Microvessel Endothelial Cells
Abstract: Endothelin-1 (ET-1), originally characterized as a potent vasoconstrictor peptide secreted by vascular endothelial cells, has now been described to possess a wide range of biological activities within the cardiovascular system and in other organs. Brain microvessel endothelial cells, which...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Fédérici, C. [verfasserIn] Camoin, L. [verfasserIn] Créminon, C. [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 1995 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2002 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 64(1995), 3, Seite 0 |
| Übergeordnetes Werk: |
volume:64 ; year:1995 ; number:3 ; pages:0 |
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| DOI / URN: |
10.1046/j.1471-4159.1995.64031008.x |
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| 520 | |a Abstract: Endothelin-1 (ET-1), originally characterized as a potent vasoconstrictor peptide secreted by vascular endothelial cells, has now been described to possess a wide range of biological activities within the cardiovascular system and in other organs. Brain microvessel endothelial cells, which, together with perivascular astrocytes, constitute the blood-brain barrier, have been shown to secrete ET-1, whereas specific ET-1 receptors are expressed on astrocytes. It is reported here that conditioned medium from primary cultures of mouse embryo astrocytes could significantly, and reversibly, attenuate the accumulation of both ET-1 and its precursor big ET-1 in the supernatant of rat brain microvessel endothelial cells by up to 59 and 76%, respectively, as assessed by immunometric assay. This inhibitor of ET-1 production was purified by gel-exclusion and ion-exchange chromatography as a 280-Da iron-containing molecule, able to release nitrites upon degradation. These results suggest that astrocytes, via release of an iron-nitrogen oxide complex, may be involved in a regulatory loop of ET-1 production at the level of the blood-brain barrier. | ||
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10.1046/j.1471-4159.1995.64031008.x doi (DE-627)NLEJ240237099 DE-627 ger DE-627 rakwb Fédérici, C. verfasserin aut Cultured Astrocytes Release a Factor that Decreases Endothelin-1 Secretion by Brain Microvessel Endothelial Cells Oxford, UK Blackwell Science Ltd 1995 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: Endothelin-1 (ET-1), originally characterized as a potent vasoconstrictor peptide secreted by vascular endothelial cells, has now been described to possess a wide range of biological activities within the cardiovascular system and in other organs. Brain microvessel endothelial cells, which, together with perivascular astrocytes, constitute the blood-brain barrier, have been shown to secrete ET-1, whereas specific ET-1 receptors are expressed on astrocytes. It is reported here that conditioned medium from primary cultures of mouse embryo astrocytes could significantly, and reversibly, attenuate the accumulation of both ET-1 and its precursor big ET-1 in the supernatant of rat brain microvessel endothelial cells by up to 59 and 76%, respectively, as assessed by immunometric assay. This inhibitor of ET-1 production was purified by gel-exclusion and ion-exchange chromatography as a 280-Da iron-containing molecule, able to release nitrites upon degradation. These results suggest that astrocytes, via release of an iron-nitrogen oxide complex, may be involved in a regulatory loop of ET-1 production at the level of the blood-brain barrier. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Endothelin Camoin, L. verfasserin aut Créminon, C. verfasserin aut Chaverot, N. oth Strosberg, A. D. oth Couraud, P. O. oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 64(1995), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:64 year:1995 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1995.64031008.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 64 1995 3 0 |
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10.1046/j.1471-4159.1995.64031008.x doi (DE-627)NLEJ240237099 DE-627 ger DE-627 rakwb Fédérici, C. verfasserin aut Cultured Astrocytes Release a Factor that Decreases Endothelin-1 Secretion by Brain Microvessel Endothelial Cells Oxford, UK Blackwell Science Ltd 1995 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: Endothelin-1 (ET-1), originally characterized as a potent vasoconstrictor peptide secreted by vascular endothelial cells, has now been described to possess a wide range of biological activities within the cardiovascular system and in other organs. Brain microvessel endothelial cells, which, together with perivascular astrocytes, constitute the blood-brain barrier, have been shown to secrete ET-1, whereas specific ET-1 receptors are expressed on astrocytes. It is reported here that conditioned medium from primary cultures of mouse embryo astrocytes could significantly, and reversibly, attenuate the accumulation of both ET-1 and its precursor big ET-1 in the supernatant of rat brain microvessel endothelial cells by up to 59 and 76%, respectively, as assessed by immunometric assay. This inhibitor of ET-1 production was purified by gel-exclusion and ion-exchange chromatography as a 280-Da iron-containing molecule, able to release nitrites upon degradation. These results suggest that astrocytes, via release of an iron-nitrogen oxide complex, may be involved in a regulatory loop of ET-1 production at the level of the blood-brain barrier. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Endothelin Camoin, L. verfasserin aut Créminon, C. verfasserin aut Chaverot, N. oth Strosberg, A. D. oth Couraud, P. O. oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 64(1995), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:64 year:1995 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1995.64031008.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 64 1995 3 0 |
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10.1046/j.1471-4159.1995.64031008.x doi (DE-627)NLEJ240237099 DE-627 ger DE-627 rakwb Fédérici, C. verfasserin aut Cultured Astrocytes Release a Factor that Decreases Endothelin-1 Secretion by Brain Microvessel Endothelial Cells Oxford, UK Blackwell Science Ltd 1995 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: Endothelin-1 (ET-1), originally characterized as a potent vasoconstrictor peptide secreted by vascular endothelial cells, has now been described to possess a wide range of biological activities within the cardiovascular system and in other organs. Brain microvessel endothelial cells, which, together with perivascular astrocytes, constitute the blood-brain barrier, have been shown to secrete ET-1, whereas specific ET-1 receptors are expressed on astrocytes. It is reported here that conditioned medium from primary cultures of mouse embryo astrocytes could significantly, and reversibly, attenuate the accumulation of both ET-1 and its precursor big ET-1 in the supernatant of rat brain microvessel endothelial cells by up to 59 and 76%, respectively, as assessed by immunometric assay. This inhibitor of ET-1 production was purified by gel-exclusion and ion-exchange chromatography as a 280-Da iron-containing molecule, able to release nitrites upon degradation. These results suggest that astrocytes, via release of an iron-nitrogen oxide complex, may be involved in a regulatory loop of ET-1 production at the level of the blood-brain barrier. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Endothelin Camoin, L. verfasserin aut Créminon, C. verfasserin aut Chaverot, N. oth Strosberg, A. D. oth Couraud, P. O. oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 64(1995), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:64 year:1995 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1995.64031008.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 64 1995 3 0 |
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10.1046/j.1471-4159.1995.64031008.x doi (DE-627)NLEJ240237099 DE-627 ger DE-627 rakwb Fédérici, C. verfasserin aut Cultured Astrocytes Release a Factor that Decreases Endothelin-1 Secretion by Brain Microvessel Endothelial Cells Oxford, UK Blackwell Science Ltd 1995 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: Endothelin-1 (ET-1), originally characterized as a potent vasoconstrictor peptide secreted by vascular endothelial cells, has now been described to possess a wide range of biological activities within the cardiovascular system and in other organs. Brain microvessel endothelial cells, which, together with perivascular astrocytes, constitute the blood-brain barrier, have been shown to secrete ET-1, whereas specific ET-1 receptors are expressed on astrocytes. It is reported here that conditioned medium from primary cultures of mouse embryo astrocytes could significantly, and reversibly, attenuate the accumulation of both ET-1 and its precursor big ET-1 in the supernatant of rat brain microvessel endothelial cells by up to 59 and 76%, respectively, as assessed by immunometric assay. This inhibitor of ET-1 production was purified by gel-exclusion and ion-exchange chromatography as a 280-Da iron-containing molecule, able to release nitrites upon degradation. These results suggest that astrocytes, via release of an iron-nitrogen oxide complex, may be involved in a regulatory loop of ET-1 production at the level of the blood-brain barrier. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Endothelin Camoin, L. verfasserin aut Créminon, C. verfasserin aut Chaverot, N. oth Strosberg, A. D. oth Couraud, P. O. oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 64(1995), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:64 year:1995 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1995.64031008.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 64 1995 3 0 |
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10.1046/j.1471-4159.1995.64031008.x doi (DE-627)NLEJ240237099 DE-627 ger DE-627 rakwb Fédérici, C. verfasserin aut Cultured Astrocytes Release a Factor that Decreases Endothelin-1 Secretion by Brain Microvessel Endothelial Cells Oxford, UK Blackwell Science Ltd 1995 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: Endothelin-1 (ET-1), originally characterized as a potent vasoconstrictor peptide secreted by vascular endothelial cells, has now been described to possess a wide range of biological activities within the cardiovascular system and in other organs. Brain microvessel endothelial cells, which, together with perivascular astrocytes, constitute the blood-brain barrier, have been shown to secrete ET-1, whereas specific ET-1 receptors are expressed on astrocytes. It is reported here that conditioned medium from primary cultures of mouse embryo astrocytes could significantly, and reversibly, attenuate the accumulation of both ET-1 and its precursor big ET-1 in the supernatant of rat brain microvessel endothelial cells by up to 59 and 76%, respectively, as assessed by immunometric assay. This inhibitor of ET-1 production was purified by gel-exclusion and ion-exchange chromatography as a 280-Da iron-containing molecule, able to release nitrites upon degradation. These results suggest that astrocytes, via release of an iron-nitrogen oxide complex, may be involved in a regulatory loop of ET-1 production at the level of the blood-brain barrier. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Endothelin Camoin, L. verfasserin aut Créminon, C. verfasserin aut Chaverot, N. oth Strosberg, A. D. oth Couraud, P. O. oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 64(1995), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:64 year:1995 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1995.64031008.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 64 1995 3 0 |
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Cultured Astrocytes Release a Factor that Decreases Endothelin-1 Secretion by Brain Microvessel Endothelial Cells |
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Abstract: Endothelin-1 (ET-1), originally characterized as a potent vasoconstrictor peptide secreted by vascular endothelial cells, has now been described to possess a wide range of biological activities within the cardiovascular system and in other organs. Brain microvessel endothelial cells, which, together with perivascular astrocytes, constitute the blood-brain barrier, have been shown to secrete ET-1, whereas specific ET-1 receptors are expressed on astrocytes. It is reported here that conditioned medium from primary cultures of mouse embryo astrocytes could significantly, and reversibly, attenuate the accumulation of both ET-1 and its precursor big ET-1 in the supernatant of rat brain microvessel endothelial cells by up to 59 and 76%, respectively, as assessed by immunometric assay. This inhibitor of ET-1 production was purified by gel-exclusion and ion-exchange chromatography as a 280-Da iron-containing molecule, able to release nitrites upon degradation. These results suggest that astrocytes, via release of an iron-nitrogen oxide complex, may be involved in a regulatory loop of ET-1 production at the level of the blood-brain barrier. |
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Abstract: Endothelin-1 (ET-1), originally characterized as a potent vasoconstrictor peptide secreted by vascular endothelial cells, has now been described to possess a wide range of biological activities within the cardiovascular system and in other organs. Brain microvessel endothelial cells, which, together with perivascular astrocytes, constitute the blood-brain barrier, have been shown to secrete ET-1, whereas specific ET-1 receptors are expressed on astrocytes. It is reported here that conditioned medium from primary cultures of mouse embryo astrocytes could significantly, and reversibly, attenuate the accumulation of both ET-1 and its precursor big ET-1 in the supernatant of rat brain microvessel endothelial cells by up to 59 and 76%, respectively, as assessed by immunometric assay. This inhibitor of ET-1 production was purified by gel-exclusion and ion-exchange chromatography as a 280-Da iron-containing molecule, able to release nitrites upon degradation. These results suggest that astrocytes, via release of an iron-nitrogen oxide complex, may be involved in a regulatory loop of ET-1 production at the level of the blood-brain barrier. |
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Abstract: Endothelin-1 (ET-1), originally characterized as a potent vasoconstrictor peptide secreted by vascular endothelial cells, has now been described to possess a wide range of biological activities within the cardiovascular system and in other organs. Brain microvessel endothelial cells, which, together with perivascular astrocytes, constitute the blood-brain barrier, have been shown to secrete ET-1, whereas specific ET-1 receptors are expressed on astrocytes. It is reported here that conditioned medium from primary cultures of mouse embryo astrocytes could significantly, and reversibly, attenuate the accumulation of both ET-1 and its precursor big ET-1 in the supernatant of rat brain microvessel endothelial cells by up to 59 and 76%, respectively, as assessed by immunometric assay. This inhibitor of ET-1 production was purified by gel-exclusion and ion-exchange chromatography as a 280-Da iron-containing molecule, able to release nitrites upon degradation. These results suggest that astrocytes, via release of an iron-nitrogen oxide complex, may be involved in a regulatory loop of ET-1 production at the level of the blood-brain barrier. |
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Cultured Astrocytes Release a Factor that Decreases Endothelin-1 Secretion by Brain Microvessel Endothelial Cells |
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Camoin, L. Créminon, C. Chaverot, N. Strosberg, A. D. Couraud, P. O. |
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