Hypoxia-induced differential apoptosis in the central nervous system of the sturgeon (Acipenser shrenckii).
Identifieur interne : 000504 ( PubMed/Checkpoint ); précédent : 000503; suivant : 000505Hypoxia-induced differential apoptosis in the central nervous system of the sturgeon (Acipenser shrenckii).
Auteurs : Gang Lu [République populaire de Chine] ; Ying T. Mak ; Sen Mun Wai ; Wai H. Kwong ; Marong Fang ; Anthony James ; David Randall ; David T. YewSource :
- Microscopy research and technique [ 1059-910X ] ; 2005.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Caspases.
- chemical : Caspase 3.
- cytology : Brain, Central Nervous System.
- pathology : Brain, Central Nervous System.
- Animals, Apoptosis, Fishes, Hypoxia, Hypoxia, Brain, In Situ Nick-End Labeling.
Abstract
Hypoxia is a frequent challenge to aquatic vertebrates as compared with that for their terrestrial counterparts. All vertebrates respond to hypoxia in a similar, but not identical manner, indicating that these responses appeared early in the evolution of vertebrates. The aim of this study is to find out the effects of hypoxia on apoptosis in the central nervous system (CNS) of sturgeon, an archaic fish. With the regional specialization of the CNS, we hypothesize that if cell death does occur, the response will vary between regions, i.e., some CNS areas will be more susceptible to hypoxia than the others would. Sturgeons (Acipenser shrenckii) were subjected to hypoxia by exposure to either air or hypoxic water. After 6- or 30-h recovery they were sacrificed and the following regions of the CNS: retina, olfactory lobe, optic tectum, pituitary, cerebellum, pons/medulla, and spinal cord were examined by the terminal transferase mediated dUTP nick end labeling technique and for the cleaved fragment of activated caspase-3 by Western blotting. In hypoxia-treated sturgeons, the retina, optic tectum, pituitary, and spinal cord were found to have significantly more apoptotic cells than did untreated sturgeons at both 6 and 30 h after the hypoxic insults, indicating prolonged damage. Apoptosis was confirmed by Western blotting of the cleaved fragment of activated caspase-3. Olfactory lobe, cerebellum, and pons/medulla had relatively few apoptotic cells. The CNS of sturgeon showed a differential pattern of apoptosis in response to hypoxia.
DOI: 10.1002/jemt.20243
PubMed: 16315235
Affiliations:
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Mak</name></author><author><name sortKey="Wai, Sen Mun" sort="Wai, Sen Mun" uniqKey="Wai S" first="Sen Mun" last="Wai">Sen Mun Wai</name></author><author><name sortKey="Kwong, Wai H" sort="Kwong, Wai H" uniqKey="Kwong W" first="Wai H" last="Kwong">Wai H. Kwong</name></author><author><name sortKey="Fang, Marong" sort="Fang, Marong" uniqKey="Fang M" first="Marong" last="Fang">Marong Fang</name></author><author><name sortKey="James, Anthony" sort="James, Anthony" uniqKey="James A" first="Anthony" last="James">Anthony James</name></author><author><name sortKey="Randall, David" sort="Randall, David" uniqKey="Randall D" first="David" last="Randall">David Randall</name></author><author><name sortKey="Yew, David T" sort="Yew, David T" uniqKey="Yew D" first="David T" last="Yew">David T. 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Mak</name></author><author><name sortKey="Wai, Sen Mun" sort="Wai, Sen Mun" uniqKey="Wai S" first="Sen Mun" last="Wai">Sen Mun Wai</name></author><author><name sortKey="Kwong, Wai H" sort="Kwong, Wai H" uniqKey="Kwong W" first="Wai H" last="Kwong">Wai H. Kwong</name></author><author><name sortKey="Fang, Marong" sort="Fang, Marong" uniqKey="Fang M" first="Marong" last="Fang">Marong Fang</name></author><author><name sortKey="James, Anthony" sort="James, Anthony" uniqKey="James A" first="Anthony" last="James">Anthony James</name></author><author><name sortKey="Randall, David" sort="Randall, David" uniqKey="Randall D" first="David" last="Randall">David Randall</name></author><author><name sortKey="Yew, David T" sort="Yew, David T" uniqKey="Yew D" first="David T" last="Yew">David T. Yew</name></author></analytic><series><title level="j">Microscopy research and technique</title><idno type="ISSN">1059-910X</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Brain (cytology)</term><term>Brain (pathology)</term><term>Caspase 3</term><term>Caspases (metabolism)</term><term>Central Nervous System (cytology)</term><term>Central Nervous System (pathology)</term><term>Fishes</term><term>Hypoxia</term><term>Hypoxia, Brain</term><term>In Situ Nick-End Labeling</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspases</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Caspase 3</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Brain</term><term>Central Nervous System</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Central Nervous System</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Fishes</term><term>Hypoxia</term><term>Hypoxia, Brain</term><term>In Situ Nick-End Labeling</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Hypoxia is a frequent challenge to aquatic vertebrates as compared with that for their terrestrial counterparts. All vertebrates respond to hypoxia in a similar, but not identical manner, indicating that these responses appeared early in the evolution of vertebrates. The aim of this study is to find out the effects of hypoxia on apoptosis in the central nervous system (CNS) of sturgeon, an archaic fish. With the regional specialization of the CNS, we hypothesize that if cell death does occur, the response will vary between regions, i.e., some CNS areas will be more susceptible to hypoxia than the others would. Sturgeons (Acipenser shrenckii) were subjected to hypoxia by exposure to either air or hypoxic water. After 6- or 30-h recovery they were sacrificed and the following regions of the CNS: retina, olfactory lobe, optic tectum, pituitary, cerebellum, pons/medulla, and spinal cord were examined by the terminal transferase mediated dUTP nick end labeling technique and for the cleaved fragment of activated caspase-3 by Western blotting. In hypoxia-treated sturgeons, the retina, optic tectum, pituitary, and spinal cord were found to have significantly more apoptotic cells than did untreated sturgeons at both 6 and 30 h after the hypoxic insults, indicating prolonged damage. Apoptosis was confirmed by Western blotting of the cleaved fragment of activated caspase-3. Olfactory lobe, cerebellum, and pons/medulla had relatively few apoptotic cells. The CNS of sturgeon showed a differential pattern of apoptosis in response to hypoxia.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16315235</PMID><DateCreated><Year>2005</Year><Month>12</Month><Day>05</Day></DateCreated><DateCompleted><Year>2006</Year><Month>01</Month><Day>26</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1059-910X</ISSN><JournalIssue CitedMedium="Print"><Volume>68</Volume><Issue>5</Issue><PubDate><Year>2005</Year><Month>Dec</Month><Day>01</Day></PubDate></JournalIssue><Title>Microscopy research and technique</Title><ISOAbbreviation>Microsc. Res. Tech.</ISOAbbreviation></Journal><ArticleTitle>Hypoxia-induced differential apoptosis in the central nervous system of the sturgeon (Acipenser shrenckii).</ArticleTitle><Pagination><MedlinePgn>258-63</MedlinePgn></Pagination><Abstract><AbstractText>Hypoxia is a frequent challenge to aquatic vertebrates as compared with that for their terrestrial counterparts. All vertebrates respond to hypoxia in a similar, but not identical manner, indicating that these responses appeared early in the evolution of vertebrates. The aim of this study is to find out the effects of hypoxia on apoptosis in the central nervous system (CNS) of sturgeon, an archaic fish. With the regional specialization of the CNS, we hypothesize that if cell death does occur, the response will vary between regions, i.e., some CNS areas will be more susceptible to hypoxia than the others would. Sturgeons (Acipenser shrenckii) were subjected to hypoxia by exposure to either air or hypoxic water. After 6- or 30-h recovery they were sacrificed and the following regions of the CNS: retina, olfactory lobe, optic tectum, pituitary, cerebellum, pons/medulla, and spinal cord were examined by the terminal transferase mediated dUTP nick end labeling technique and for the cleaved fragment of activated caspase-3 by Western blotting. In hypoxia-treated sturgeons, the retina, optic tectum, pituitary, and spinal cord were found to have significantly more apoptotic cells than did untreated sturgeons at both 6 and 30 h after the hypoxic insults, indicating prolonged damage. Apoptosis was confirmed by Western blotting of the cleaved fragment of activated caspase-3. Olfactory lobe, cerebellum, and pons/medulla had relatively few apoptotic cells. The CNS of sturgeon showed a differential pattern of apoptosis in response to hypoxia.</AbstractText><CopyrightInformation>(c) 2005 Wiley-Liss, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Gang</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Anatomy, Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mak</LastName><ForeName>Ying T</ForeName><Initials>YT</Initials></Author><Author ValidYN="Y"><LastName>Wai</LastName><ForeName>Sen Mun</ForeName><Initials>SM</Initials></Author><Author ValidYN="Y"><LastName>Kwong</LastName><ForeName>Wai H</ForeName><Initials>WH</Initials></Author><Author ValidYN="Y"><LastName>Fang</LastName><ForeName>Marong</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>James</LastName><ForeName>Anthony</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Randall</LastName><ForeName>David</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Yew</LastName><ForeName>David T</ForeName><Initials>DT</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Microsc Res Tech</MedlineTA><NlmUniqueID>9203012</NlmUniqueID><ISSNLinking>1059-910X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D053148">Caspase 3</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D020169">Caspases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="Y">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053148" MajorTopicYN="N">Caspase 3</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020169" MajorTopicYN="N">Caspases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002490" MajorTopicYN="N">Central Nervous System</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005399" MajorTopicYN="N">Fishes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000860" MajorTopicYN="Y">Hypoxia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002534" MajorTopicYN="N">Hypoxia, Brain</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020287" MajorTopicYN="N">In Situ Nick-End Labeling</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>11</Month><Day>30</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>1</Month><Day>27</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>11</Month><Day>30</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16315235</ArticleId><ArticleId IdType="doi">10.1002/jemt.20243</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country><settlement><li>Sha Tin</li></settlement><orgName><li>Université chinoise de Hong Kong</li></orgName></list><tree><noCountry><name sortKey="Fang, Marong" sort="Fang, Marong" uniqKey="Fang M" first="Marong" last="Fang">Marong Fang</name><name sortKey="James, Anthony" sort="James, Anthony" uniqKey="James A" first="Anthony" last="James">Anthony James</name><name sortKey="Kwong, Wai H" sort="Kwong, Wai H" uniqKey="Kwong W" first="Wai H" last="Kwong">Wai H. Kwong</name><name sortKey="Mak, Ying T" sort="Mak, Ying T" uniqKey="Mak Y" first="Ying T" last="Mak">Ying T. Mak</name><name sortKey="Randall, David" sort="Randall, David" uniqKey="Randall D" first="David" last="Randall">David Randall</name><name sortKey="Wai, Sen Mun" sort="Wai, Sen Mun" uniqKey="Wai S" first="Sen Mun" last="Wai">Sen Mun Wai</name><name sortKey="Yew, David T" sort="Yew, David T" uniqKey="Yew D" first="David T" last="Yew">David T. Yew</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Lu, Gang" sort="Lu, Gang" uniqKey="Lu G" first="Gang" last="Lu">Gang Lu</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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