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Activation of C-Jun N-terminal kinase is required for glutathione transferase A4 induction during oxidative stress, not during cell proliferation, in mouse hepatocytes

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Title: Activation of C-Jun N-terminal kinase is required for glutathione transferase A4 induction during oxidative stress, not during cell proliferation, in mouse hepatocytes
Authors: Desmots, Fabienne1, Loyer, Pascal2, Rissel, Maryvonne1, Guillouzo, André1, Morel, Fabrice1 fabrice.morel@rennes.inserm.fr
Source: FEBS Letters. Oct2005, Vol. 579 Issue 25, p5691-5696. 6p.
Subjects: Epidermal growth factor, Glutathione transferase, Transferases, Glutathione
Abstract: Abstract: Expression of the mouse glutathione transferase Alpha 4 (mGSTA4) has been studied during hepatocyte isolation and in cultured hepatocytes. Transient mGSTA4 induction during liver disruption correlated to strong oxidative stress and induction of the Jun N-terminal kinase (JNK) pathway. Similarly, tumor necrosis factor α induced both JNK phosphorylation and mGSTA4 expression while specific JNK inhibitor JNKI1 prevented these two events and JNK activator anisomycin strongly induced mGSTA4 expression. We also found that endogenous JNK and mGSTA4 co-immunoprecipitate. A second mGSTA4 induction occurred 2 days after cell seeding concomitantly to DNA replication and was prevented by treatment with mitogen-activated protein kinase (MEK) inhibitor U0126. Our data demonstrate that mGSTA4 is strongly increased during oxidative stress possibly via JNK pathway and during proliferation via MEK/extracellular signal-regulated kinase pathway, and suggest that mGSTA4 might be an endogenous regulator of JNK activity by direct binding. [Copyright &y& Elsevier]
Copyright of FEBS Letters is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Engineering Source
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Header DbId: egs
DbLabel: Engineering Source
An: 18782005
AccessLevel: 6
PubType: Academic Journal
PubTypeId: academicJournal
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  Data: Activation of C-Jun N-terminal kinase is required for glutathione transferase A4 induction during oxidative stress, not during cell proliferation, in mouse hepatocytes
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  Data: <searchLink fieldCode="AR" term="%22Desmots%2C+Fabienne%22">Desmots, Fabienne</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Loyer%2C+Pascal%22">Loyer, Pascal</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Rissel%2C+Maryvonne%22">Rissel, Maryvonne</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Guillouzo%2C+André%22">Guillouzo, André</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Morel%2C+Fabrice%22">Morel, Fabrice</searchLink><relatesTo>1</relatesTo><i> fabrice.morel@rennes.inserm.fr</i>
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  Data: <searchLink fieldCode="JN" term="%22FEBS+Letters%22">FEBS Letters</searchLink>. Oct2005, Vol. 579 Issue 25, p5691-5696. 6p.
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  Data: <searchLink fieldCode="DE" term="%22Epidermal+growth+factor%22">Epidermal growth factor</searchLink><br /><searchLink fieldCode="DE" term="%22Glutathione+transferase%22">Glutathione transferase</searchLink><br /><searchLink fieldCode="DE" term="%22Transferases%22">Transferases</searchLink><br /><searchLink fieldCode="DE" term="%22Glutathione%22">Glutathione</searchLink>
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  Label: Abstract
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  Data: Abstract: Expression of the mouse glutathione transferase Alpha 4 (mGSTA4) has been studied during hepatocyte isolation and in cultured hepatocytes. Transient mGSTA4 induction during liver disruption correlated to strong oxidative stress and induction of the Jun N-terminal kinase (JNK) pathway. Similarly, tumor necrosis factor α induced both JNK phosphorylation and mGSTA4 expression while specific JNK inhibitor JNKI1 prevented these two events and JNK activator anisomycin strongly induced mGSTA4 expression. We also found that endogenous JNK and mGSTA4 co-immunoprecipitate. A second mGSTA4 induction occurred 2 days after cell seeding concomitantly to DNA replication and was prevented by treatment with mitogen-activated protein kinase (MEK) inhibitor U0126. Our data demonstrate that mGSTA4 is strongly increased during oxidative stress possibly via JNK pathway and during proliferation via MEK/extracellular signal-regulated kinase pathway, and suggest that mGSTA4 might be an endogenous regulator of JNK activity by direct binding. [Copyright &y& Elsevier]
– Name: AbstractSuppliedCopyright
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  Data: <i>Copyright of FEBS Letters is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1016/j.febslet.2005.08.088
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      – Code: eng
        Text: English
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        Type: general
      – SubjectFull: Glutathione transferase
        Type: general
      – SubjectFull: Transferases
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      – SubjectFull: Glutathione
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      – TitleFull: Activation of C-Jun N-terminal kinase is required for glutathione transferase A4 induction during oxidative stress, not during cell proliferation, in mouse hepatocytes
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              Text: Oct2005
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