ParkinsonFranceV1, PascalFrancis, Curation, bibRecord, 000234

6-hydroxydopamine-induced nuclear factor-kappab activation in PC12 cells

Identifieur interne : 000234 ( PascalFrancis/Curation ); précédent : 000233; suivant : 000235

6-hydroxydopamine-induced nuclear factor-kappab activation in PC12 cells

Auteurs : David Blum [Belgique, France] ; Sakina Torch [France] ; Marie-France Nissou [France] ; Jean-Marc Verna [France]

Source :

Biochemical pharmacology [ 0006-2952 ] ; 2001.

RBID : Pascal:01-0372250

Descripteurs français

Pascal (Inist)
- Oxidopamine, Sympathomimétique, Neurotoxine, Mort cellulaire, Lignée cellulaire établie, Stress oxydatif, Parkinson maladie, Homme, Dopamine, Activation, Toxicité, Expression génique, Catécholamine, Neurone, Lignée PC12, Facteur transcription NFκB.
Wicri :
- topic : Homme.

English descriptors

KwdEn :
- Activation, Catecholamine, Cell death, Dopamine, Established cell line, Gene expression, Human, Neuron, Neurotoxin, Oxidative stress, Oxidopamine, Parkinson disease, Sympathomimetic, Toxicity, Transcription factor NFκB.

Abstract

The involvement of nuclear Factor-kappaB (NF-κB) transcription factor in PC12 cell death triggered by the dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA) was investigated. Results show that oxidative stress generated by 6-OHDA activates NF-KB. When the NF-KB activation was inhibited by parthenolide. PC12 cell death induced by 6-OHDA was significantly increased, thus suggesting an involvement of this transcription factor in a protective mechanism against 6-OHDA toxicity. To further assess this hypothesis, we studied the involvement of NF-KB in the protective effect of two anti-apoptotic genes, bcl-2 and bfl-1 Although Bcl-2 and Bfl- I expression normally protects PC12 cells from 6-OHDA, parthenolide strongly decreased the beneficial effects afforded by transgene expression. These results suggest: (1) that the transcription factor NF-KB is likely associated with the protection of catecholaminergic PC12 cells and (2) that the protective effects afforded by bcl-2 and bfl-1 expression may be dependent on NF-KB activation.

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A03		`1`		`@0 Biochem. pharmacol.`
A05				`@2 62`
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A08	`01`	`1`	`ENG`	`@1 6-hydroxydopamine-induced nuclear factor-kappab activation in PC12 cells`
A11	`01`	`1`		`@1 BLUM (David)`
A11	`02`	`1`		`@1 TORCH (Sakina)`
A11	`03`	`1`		`@1 NISSOU (Marie-France)`
A11	`04`	`1`		`@1 VERNA (Jean-Marc)`
A14	`01`			`@1 Laboratoire de Neurophysiologie, Département de Neurosciences, ULB-Erasme, 808 route de Lennik, CP601 @2 1070 Bruxelles @3 BEL @Z 1 aut.`
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A20				`@1 473-481`
A21				`@1 2001`
A23	`01`			`@0 ENG`
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A44				`@0 0000 @1 © 2001 INIST-CNRS. All rights reserved.`
A45				`@0 59 ref.`
A47	`01`	`1`		`@0 01-0372250`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Biochemical pharmacology`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 The involvement of nuclear Factor-kappaB (NF-κB) transcription factor in PC12 cell death triggered by the dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA) was investigated. Results show that oxidative stress generated by 6-OHDA activates NF-KB. When the NF-KB activation was inhibited by parthenolide. PC12 cell death induced by 6-OHDA was significantly increased, thus suggesting an involvement of this transcription factor in a protective mechanism against 6-OHDA toxicity. To further assess this hypothesis, we studied the involvement of NF-KB in the protective effect of two anti-apoptotic genes, bcl-2 and bfl-1 Although Bcl-2 and Bfl- I expression normally protects PC12 cells from 6-OHDA, parthenolide strongly decreased the beneficial effects afforded by transgene expression. These results suggest: (1) that the transcription factor NF-KB is likely associated with the protection of catecholaminergic PC12 cells and (2) that the protective effects afforded by bcl-2 and bfl-1 expression may be dependent on NF-KB activation.
C02	`01`	`X`		`@0 002B02U01`
C03	`01`	`X`	`FRE`	`@0 Oxidopamine @2 NK @2 FR @5 01`
C03	`01`	`X`	`ENG`	`@0 Oxidopamine @2 NK @2 FR @5 01`
C03	`01`	`X`	`SPA`	`@0 Oxidopamina @2 NK @2 FR @5 01`
C03	`02`	`X`	`FRE`	`@0 Sympathomimétique @5 04`
C03	`02`	`X`	`ENG`	`@0 Sympathomimetic @5 04`
C03	`02`	`X`	`SPA`	`@0 Simpaticomimético @5 04`
C03	`03`	`X`	`FRE`	`@0 Neurotoxine @5 07`
C03	`03`	`X`	`ENG`	`@0 Neurotoxin @5 07`
C03	`03`	`X`	`SPA`	`@0 Neurotoxina @5 07`
C03	`04`	`X`	`FRE`	`@0 Mort cellulaire @5 10`
C03	`04`	`X`	`ENG`	`@0 Cell death @5 10`
C03	`04`	`X`	`SPA`	`@0 Muerte celular @5 10`
C03	`05`	`X`	`FRE`	`@0 Lignée cellulaire établie @5 11`
C03	`05`	`X`	`ENG`	`@0 Established cell line @5 11`
C03	`05`	`X`	`SPA`	`@0 Línea celular establecida @5 11`
C03	`06`	`X`	`FRE`	`@0 Stress oxydatif @5 12`
C03	`06`	`X`	`ENG`	`@0 Oxidative stress @5 12`
C03	`06`	`X`	`SPA`	`@0 Stress oxidativo @5 12`
C03	`07`	`X`	`FRE`	`@0 Parkinson maladie @5 13`
C03	`07`	`X`	`ENG`	`@0 Parkinson disease @5 13`
C03	`07`	`X`	`SPA`	`@0 Parkinson enfermedad @5 13`
C03	`08`	`X`	`FRE`	`@0 Homme @5 14`
C03	`08`	`X`	`ENG`	`@0 Human @5 14`
C03	`08`	`X`	`SPA`	`@0 Hombre @5 14`
C03	`09`	`X`	`FRE`	`@0 Dopamine @2 NK @2 FR @5 15`
C03	`09`	`X`	`ENG`	`@0 Dopamine @2 NK @2 FR @5 15`
C03	`09`	`X`	`SPA`	`@0 Dopamina @2 NK @2 FR @5 15`
C03	`10`	`X`	`FRE`	`@0 Activation @5 16`
C03	`10`	`X`	`ENG`	`@0 Activation @5 16`
C03	`10`	`X`	`SPA`	`@0 Activación @5 16`
C03	`11`	`X`	`FRE`	`@0 Toxicité @5 17`
C03	`11`	`X`	`ENG`	`@0 Toxicity @5 17`
C03	`11`	`X`	`SPA`	`@0 Toxicidad @5 17`
C03	`12`	`X`	`FRE`	`@0 Expression génique @5 18`
C03	`12`	`X`	`ENG`	`@0 Gene expression @5 18`
C03	`12`	`X`	`SPA`	`@0 Expresión genética @5 18`
C03	`13`	`X`	`FRE`	`@0 Catécholamine @5 20`
C03	`13`	`X`	`ENG`	`@0 Catecholamine @5 20`
C03	`13`	`X`	`SPA`	`@0 Catecolamina @5 20`
C03	`14`	`X`	`FRE`	`@0 Neurone @5 21`
C03	`14`	`X`	`ENG`	`@0 Neuron @5 21`
C03	`14`	`X`	`SPA`	`@0 Neurona @5 21`
C03	`15`	`X`	`FRE`	`@0 Lignée PC12 @4 INC @5 89`
C03	`16`	`X`	`FRE`	`@0 Facteur transcription NFκB @4 CD @5 96`
C03	`16`	`X`	`ENG`	`@0 Transcription factor NFκB @4 CD @5 96`
C07	`01`	`X`	`FRE`	`@0 Système nerveux pathologie @5 69`
C07	`01`	`X`	`ENG`	`@0 Nervous system diseases @5 69`
C07	`01`	`X`	`SPA`	`@0 Sistema nervioso patología @5 69`
C07	`02`	`X`	`FRE`	`@0 Système nerveux central pathologie @5 70`
C07	`02`	`X`	`ENG`	`@0 Central nervous system disease @5 70`
C07	`02`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 70`
C07	`03`	`X`	`FRE`	`@0 Encéphale pathologie @5 71`
C07	`03`	`X`	`ENG`	`@0 Cerebral disorder @5 71`
C07	`03`	`X`	`SPA`	`@0 Encéfalo patología @5 71`
C07	`04`	`X`	`FRE`	`@0 Extrapyramidal syndrome @5 72`
C07	`04`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 72`
C07	`04`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 72`
C07	`05`	`X`	`FRE`	`@0 Maladie dégénérative @5 73`
C07	`05`	`X`	`ENG`	`@0 Degenerative disease @5 73`
C07	`05`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 73`
N21				`@1 260`

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Pascal:01-0372250

Le document en format XML

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<term>Established cell line</term>
<term>Gene expression</term>
<term>Human</term>
<term>Neuron</term>
<term>Neurotoxin</term>
<term>Oxidative stress</term>
<term>Oxidopamine</term>
<term>Parkinson disease</term>
<term>Sympathomimetic</term>
<term>Toxicity</term>
<term>Transcription factor NFκB</term>
</keywords>
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<term>Neurotoxine</term>
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<term>Activation</term>
<term>Toxicité</term>
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<front><div type="abstract" xml:lang="en">The involvement of nuclear Factor-kappaB (NF-κB) transcription factor in PC12 cell death triggered by the dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA) was investigated. Results show that oxidative stress generated by 6-OHDA activates NF-KB. When the NF-KB activation was inhibited by parthenolide. PC12 cell death induced by 6-OHDA was significantly increased, thus suggesting an involvement of this transcription factor in a protective mechanism against 6-OHDA toxicity. To further assess this hypothesis, we studied the involvement of NF-KB in the protective effect of two anti-apoptotic genes, bcl-2 and bfl-1 Although Bcl-2 and Bfl- I expression normally protects PC12 cells from 6-OHDA, parthenolide strongly decreased the beneficial effects afforded by transgene expression. These results suggest: (1) that the transcription factor NF-KB is likely associated with the protection of catecholaminergic PC12 cells and (2) that the protective effects afforded by bcl-2 and bfl-1 expression may be dependent on NF-KB activation.</div>
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<sZ>1 aut.</sZ>
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<fC01 i1="01" l="ENG"><s0>The involvement of nuclear Factor-kappaB (NF-κB) transcription factor in PC12 cell death triggered by the dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA) was investigated. Results show that oxidative stress generated by 6-OHDA activates NF-KB. When the NF-KB activation was inhibited by parthenolide. PC12 cell death induced by 6-OHDA was significantly increased, thus suggesting an involvement of this transcription factor in a protective mechanism against 6-OHDA toxicity. To further assess this hypothesis, we studied the involvement of NF-KB in the protective effect of two anti-apoptotic genes, bcl-2 and bfl-1 Although Bcl-2 and Bfl- I expression normally protects PC12 cells from 6-OHDA, parthenolide strongly decreased the beneficial effects afforded by transgene expression. These results suggest: (1) that the transcription factor NF-KB is likely associated with the protection of catecholaminergic PC12 cells and (2) that the protective effects afforded by bcl-2 and bfl-1 expression may be dependent on NF-KB activation.</s0>
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<s5>04</s5>
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<s5>04</s5>
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<s5>04</s5>
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<fC03 i1="03" i2="X" l="FRE"><s0>Neurotoxine</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Neurotoxin</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Neurotoxina</s0>
<s5>07</s5>
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<fC03 i1="04" i2="X" l="FRE"><s0>Mort cellulaire</s0>
<s5>10</s5>
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<fC03 i1="04" i2="X" l="ENG"><s0>Cell death</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Muerte celular</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Lignée cellulaire établie</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Established cell line</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Línea celular establecida</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Stress oxydatif</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Oxidative stress</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Stress oxidativo</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Homme</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Human</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Hombre</s0>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Dopamina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>15</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Activation</s0>
<s5>16</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Activation</s0>
<s5>16</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Activación</s0>
<s5>16</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Toxicité</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Toxicity</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Toxicidad</s0>
<s5>17</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Expression génique</s0>
<s5>18</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Gene expression</s0>
<s5>18</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Expresión genética</s0>
<s5>18</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Catécholamine</s0>
<s5>20</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Catecholamine</s0>
<s5>20</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Catecolamina</s0>
<s5>20</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE"><s0>Neurone</s0>
<s5>21</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG"><s0>Neuron</s0>
<s5>21</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA"><s0>Neurona</s0>
<s5>21</s5>
</fC03>
<fC03 i1="15" i2="X" l="FRE"><s0>Lignée PC12</s0>
<s4>INC</s4>
<s5>89</s5>
</fC03>
<fC03 i1="16" i2="X" l="FRE"><s0>Facteur transcription NFκB</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="16" i2="X" l="ENG"><s0>Transcription factor NFκB</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>69</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>69</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>69</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>70</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>70</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>70</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>71</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>71</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>71</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>72</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>72</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>72</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>73</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>73</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>73</s5>
</fC07>
<fN21><s1>260</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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This area was generated with Dilib version V0.6.29.
Data generation: Wed May 17 19:46:39 2017. Site generation: Mon Mar 4 15:48:15 2024

	La maladie de Parkinson en France (serveur d'exploration)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

La maladie de Parkinson en France (serveur d'exploration)

6-hydroxydopamine-induced nuclear factor-kappab activation in PC12 cells

6-hydroxydopamine-induced nuclear factor-kappab activation in PC12 cells

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