Induction of heat shock proteins in cerebral cortical cultures by celastrol
Identifieur interne : 000213 ( Pmc/Corpus ); précédent : 000212; suivant : 000214Induction of heat shock proteins in cerebral cortical cultures by celastrol
Auteurs : Ari M. Chow ; Derek W. F. Tang ; Asad Hanif ; Ian R. BrownSource :
- Cell Stress & Chaperones [ 1355-8145 ] ; 2012.
Abstract
Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis (ALS) are ‘protein misfolding disorders’ of the mature nervous system that are characterized by the accumulation of protein aggregates and selective cell loss. Different brain regions are impacted, with Alzheimer’s affecting cells in the cerebral cortex, Parkinson’s targeting dopaminergic cells in the substantia nigra and ALS causing degeneration of cells in the spinal cord. These diseases differ widely in frequency in the human population. Alzheimer’s is more frequent than Parkinson’s and ALS. Heat shock proteins (Hsps) are ‘protein repair agents’ that provide a line of defense against misfolded, aggregation-prone proteins. We have suggested that differing levels of constitutively expressed Hsps (Hsc70 and Hsp27) in neural cell populations confer a variable buffering capacity against ‘protein misfolding disorders’ that correlates with the relative frequencies of these neurodegenerative diseases. The high relative frequency of Alzheimer’s may due to low levels of Hsc70 and Hsp27 in affected cell populations that results in a reduced defense capacity against protein misfolding. Here, we demonstrate that celastrol, but not classical heat shock treatment, is effective in inducing a set of neuroprotective Hsps in cultures derived from cerebral cortices, including Hsp70, Hsp27 and Hsp32. This set of Hsps is induced by celastrol at ‘days in vitro’ (DIV) 13 when cultured cortical cells reached maturity. The inducibility of a set of neuroprotective Hsps in mature cortical cultures at DIV13 suggests that celastrol is a potential agent to counter Alzheimer’s disease, a neurodegenerative ‘protein misfolding disorder’ of the adult brain that targets cells in the cerebral cortex.
Url:
DOI: 10.1007/s12192-012-0364-0
PubMed: 22865541
PubMed Central: 3581628
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PMC:3581628Le document en format XML
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<author><name sortKey="Hanif, Asad" sort="Hanif, Asad" uniqKey="Hanif A" first="Asad" last="Hanif">Asad Hanif</name>
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<front><div type="abstract" xml:lang="en"><p>Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis (ALS) are ‘protein misfolding disorders’ of the mature nervous system that are characterized by the accumulation of protein aggregates and selective cell loss. Different brain regions are impacted, with Alzheimer’s affecting cells in the cerebral cortex, Parkinson’s targeting dopaminergic cells in the substantia nigra and ALS causing degeneration of cells in the spinal cord. These diseases differ widely in frequency in the human population. Alzheimer’s is more frequent than Parkinson’s and ALS. Heat shock proteins (Hsps) are ‘protein repair agents’ that provide a line of defense against misfolded, aggregation-prone proteins. We have suggested that differing levels of constitutively expressed Hsps (Hsc70 and Hsp27) in neural cell populations confer a variable buffering capacity against ‘protein misfolding disorders’ that correlates with the relative frequencies of these neurodegenerative diseases. The high relative frequency of Alzheimer’s may due to low levels of Hsc70 and Hsp27 in affected cell populations that results in a reduced defense capacity against protein misfolding. Here, we demonstrate that celastrol, but not classical heat shock treatment, is effective in inducing a set of neuroprotective Hsps in cultures derived from cerebral cortices, including Hsp70, Hsp27 and Hsp32. This set of Hsps is induced by celastrol at ‘days in vitro’ (DIV) 13 when cultured cortical cells reached maturity. The inducibility of a set of neuroprotective Hsps in mature cortical cultures at DIV13 suggests that celastrol is a potential agent to counter Alzheimer’s disease, a neurodegenerative ‘protein misfolding disorder’ of the adult brain that targets cells in the cerebral cortex.</p>
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Cell Stress Chaperones</journal-id>
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<article-categories><subj-group subj-group-type="heading"><subject>Original Paper</subject>
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<title-group><article-title>Induction of heat shock proteins in cerebral cortical cultures by celastrol</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>Chow</surname>
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<given-names>Derek W. F.</given-names>
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<contrib contrib-type="author"><name><surname>Hanif</surname>
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<contrib contrib-type="author" corresp="yes"><name><surname>Brown</surname>
<given-names>Ian R.</given-names>
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<address><phone>+1-416-2877413</phone>
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<pub-date pub-type="epub"><day>3</day>
<month>8</month>
<year>2012</year>
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<pub-date pub-type="ppub"><month>3</month>
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<volume>18</volume>
<issue>2</issue>
<fpage>155</fpage>
<lpage>160</lpage>
<history><date date-type="received"><day>17</day>
<month>6</month>
<year>2012</year>
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<date date-type="rev-recd"><day>23</day>
<month>7</month>
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<date date-type="accepted"><day>24</day>
<month>7</month>
<year>2012</year>
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<permissions><copyright-statement>© Cell Stress Society International 2012</copyright-statement>
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<abstract id="Abs1"><p>Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis (ALS) are ‘protein misfolding disorders’ of the mature nervous system that are characterized by the accumulation of protein aggregates and selective cell loss. Different brain regions are impacted, with Alzheimer’s affecting cells in the cerebral cortex, Parkinson’s targeting dopaminergic cells in the substantia nigra and ALS causing degeneration of cells in the spinal cord. These diseases differ widely in frequency in the human population. Alzheimer’s is more frequent than Parkinson’s and ALS. Heat shock proteins (Hsps) are ‘protein repair agents’ that provide a line of defense against misfolded, aggregation-prone proteins. We have suggested that differing levels of constitutively expressed Hsps (Hsc70 and Hsp27) in neural cell populations confer a variable buffering capacity against ‘protein misfolding disorders’ that correlates with the relative frequencies of these neurodegenerative diseases. The high relative frequency of Alzheimer’s may due to low levels of Hsc70 and Hsp27 in affected cell populations that results in a reduced defense capacity against protein misfolding. Here, we demonstrate that celastrol, but not classical heat shock treatment, is effective in inducing a set of neuroprotective Hsps in cultures derived from cerebral cortices, including Hsp70, Hsp27 and Hsp32. This set of Hsps is induced by celastrol at ‘days in vitro’ (DIV) 13 when cultured cortical cells reached maturity. The inducibility of a set of neuroprotective Hsps in mature cortical cultures at DIV13 suggests that celastrol is a potential agent to counter Alzheimer’s disease, a neurodegenerative ‘protein misfolding disorder’ of the adult brain that targets cells in the cerebral cortex.</p>
</abstract>
<kwd-group xml:lang="en"><title>Keywords</title>
<kwd>Hsp70</kwd>
<kwd>Hsp32</kwd>
<kwd>Hsp27</kwd>
<kwd>Alzheimer’s disease</kwd>
<kwd>Celastrol</kwd>
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<meta-value>© Cell Stress Society International 2013</meta-value>
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