Involvement of the PTEN–AKT–FOXO3a Pathway in Neuronal Apoptosis in Developing Rat Brain after Hypoxia–Ischemia
The proapoptotic function of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) phosphatase has been linked to its capacity to antagonize the phosphatidylinositol-3-kinase–Akt signaling pathway. Previous studies have shown that the Forkhead transcriptional factor (FOXO3a) is a critical e...
Gespeichert in:
| Veröffentlicht in: | Journal of cerebral blood flow and metabolism 2009-12, Vol.29 (12), p.1903-1913 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1913 |
|---|---|
| container_issue | 12 |
| container_start_page | 1903 |
| container_title | Journal of cerebral blood flow and metabolism |
| container_volume | 29 |
| creator | Li, Deyuan Qu, Yi Mao, Meng Zhang, Xiaolan Li, Jinhui Ferriero, Donna Mu, Dezhi |
| description | The proapoptotic function of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) phosphatase has been linked to its capacity to antagonize the phosphatidylinositol-3-kinase–Akt signaling pathway. Previous studies have shown that the Forkhead transcriptional factor (FOXO3a) is a critical effector of the PTEN-mediated tumor suppressor. However, whether the PTEN–Akt–FOXO3a pathway is involved in neuronal apoptosis in developing rat brain after hypoxia–ischemia (HI) is unclear. In this study, we generated an HI model using postnatal day 10 rats. Immunohistochemistry and western blot were used to detect the expression of total and phosphorylated PTEN, Akt, and FOXO3a, as well as its target gene Bim. We found that dephosphorylation of PTEN was accompanied by dephosphorylation of Akt and FOXO3a, which induced FOXO3a translocation into the nucleus and upregulated the expression of Bim. Furthermore, we found that PTEN inhibition by bisperoxovanadium significantly increased the phosphorylation of Akt and FOXO3a, decreased the nuclear translocation of FOXO3a, and inhibited Bim expression after HI. Moreover, the downregulation of Bim caused by PTEN inhibition attenuated cellular apoptosis in developing rat brain. Our findings suggest that the PTEN–Akt–FOXO3a pathway is involved in neuronal apoptosis in neonatal rat brain after HI. Agents targeting PTEN may offer a promise to rescue neurons from HI brain damage. |
| doi_str_mv | 10.1038/jcbfm.2009.102 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2846558</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.1038_jcbfm.2009.102</sage_id><sourcerecordid>21226269</sourcerecordid><originalsourceid>FETCH-LOGICAL-c579t-14917a8df0dec57fb763ba0499d069eb0f58b27cdb589bf384c98e87207fcf553</originalsourceid><addsrcrecordid>eNp9kc1uEzEUhS0EoqGwZYlGSMACTfDP-G9TKZSWRlRNhYLU3cjj2ImjmfFgzwSy4x14Q54Eh0QtIMHG1j3-fHyvDwBPERwjSMSbta5sM8YQylTje2CEKJU5h4jdByOIOcoZFzdH4FGMawihIJQ-BEdIMkyQLEZgmLYbX29MY9o-8zbrVya7np9d_fj2ffJhntbz2c2MqOxa9asvapu5NrsyQ_CtqrNJ57veRxd36juzMbXvXLvMPqo-extUEpXtTcgutp3_6lQym0a9Mo1Tj8EDq-ponhz2Y_Dp_Gx-epFfzt5PTyeXuaZc9jkqJOJKLCxcmKTYijNSKVhIuYBMmgpaKirM9aKiQlaWiEJLYQTHkFttKSXH4GTv2w1VYxY6DRlUXXbBNSpsS69c-edJ61bl0m9KLApGqUgGrw4GwX8eTOzLxkVt6lq1xg-x5IQIwongiXz5XxIjjBlmMoHP_wLXfgjpP3eMLAqIGUzQeA_p4GMMxt72jGC5C778FXy5Cz7VOF149vukd_gh6QS8OAAqalXboFrt4i2HMZZUMJS413suqqW5a-0fz_4ESbrIWg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>219440260</pqid></control><display><type>article</type><title>Involvement of the PTEN–AKT–FOXO3a Pathway in Neuronal Apoptosis in Developing Rat Brain after Hypoxia–Ischemia</title><source>SAGE Complete A-Z List</source><source>MEDLINE</source><creator>Li, Deyuan ; Qu, Yi ; Mao, Meng ; Zhang, Xiaolan ; Li, Jinhui ; Ferriero, Donna ; Mu, Dezhi</creator><creatorcontrib>Li, Deyuan ; Qu, Yi ; Mao, Meng ; Zhang, Xiaolan ; Li, Jinhui ; Ferriero, Donna ; Mu, Dezhi</creatorcontrib><description>The proapoptotic function of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) phosphatase has been linked to its capacity to antagonize the phosphatidylinositol-3-kinase–Akt signaling pathway. Previous studies have shown that the Forkhead transcriptional factor (FOXO3a) is a critical effector of the PTEN-mediated tumor suppressor. However, whether the PTEN–Akt–FOXO3a pathway is involved in neuronal apoptosis in developing rat brain after hypoxia–ischemia (HI) is unclear. In this study, we generated an HI model using postnatal day 10 rats. Immunohistochemistry and western blot were used to detect the expression of total and phosphorylated PTEN, Akt, and FOXO3a, as well as its target gene Bim. We found that dephosphorylation of PTEN was accompanied by dephosphorylation of Akt and FOXO3a, which induced FOXO3a translocation into the nucleus and upregulated the expression of Bim. Furthermore, we found that PTEN inhibition by bisperoxovanadium significantly increased the phosphorylation of Akt and FOXO3a, decreased the nuclear translocation of FOXO3a, and inhibited Bim expression after HI. Moreover, the downregulation of Bim caused by PTEN inhibition attenuated cellular apoptosis in developing rat brain. Our findings suggest that the PTEN–Akt–FOXO3a pathway is involved in neuronal apoptosis in neonatal rat brain after HI. Agents targeting PTEN may offer a promise to rescue neurons from HI brain damage.</description><identifier>ISSN: 0271-678X</identifier><identifier>EISSN: 1559-7016</identifier><identifier>DOI: 10.1038/jcbfm.2009.102</identifier><identifier>PMID: 19623194</identifier><identifier>CODEN: JCBMDN</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Animals ; Apoptosis ; Apoptosis Regulatory Proteins - genetics ; Apoptosis Regulatory Proteins - metabolism ; Bcl-2-Like Protein 11 ; Biological and medical sciences ; Cell Nucleus - metabolism ; Cytoplasm - metabolism ; Enzyme Inhibitors - pharmacology ; Female ; Forkhead Box Protein O3 ; Forkhead Transcription Factors - genetics ; Forkhead Transcription Factors - metabolism ; Gene Expression ; Hypoxia-Ischemia, Brain - metabolism ; Medical sciences ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Neurology ; Neurons - cytology ; Neuropharmacology ; Neuroprotective agent ; Pharmacology. Drug treatments ; Phosphorylation ; Protein Transport ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; PTEN Phosphohydrolase - antagonists & inhibitors ; PTEN Phosphohydrolase - genetics ; PTEN Phosphohydrolase - metabolism ; Rats ; Rats, Sprague-Dawley ; Vanadium Compounds - pharmacology ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Journal of cerebral blood flow and metabolism, 2009-12, Vol.29 (12), p.1903-1913</ispartof><rights>2009 ISCBFM</rights><rights>2015 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Dec 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c579t-14917a8df0dec57fb763ba0499d069eb0f58b27cdb589bf384c98e87207fcf553</citedby><cites>FETCH-LOGICAL-c579t-14917a8df0dec57fb763ba0499d069eb0f58b27cdb589bf384c98e87207fcf553</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1038/jcbfm.2009.102$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1038/jcbfm.2009.102$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>230,314,776,780,881,21798,27901,27902,43597,43598</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22295861$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19623194$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Deyuan</creatorcontrib><creatorcontrib>Qu, Yi</creatorcontrib><creatorcontrib>Mao, Meng</creatorcontrib><creatorcontrib>Zhang, Xiaolan</creatorcontrib><creatorcontrib>Li, Jinhui</creatorcontrib><creatorcontrib>Ferriero, Donna</creatorcontrib><creatorcontrib>Mu, Dezhi</creatorcontrib><title>Involvement of the PTEN–AKT–FOXO3a Pathway in Neuronal Apoptosis in Developing Rat Brain after Hypoxia–Ischemia</title><title>Journal of cerebral blood flow and metabolism</title><addtitle>J Cereb Blood Flow Metab</addtitle><description>The proapoptotic function of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) phosphatase has been linked to its capacity to antagonize the phosphatidylinositol-3-kinase–Akt signaling pathway. Previous studies have shown that the Forkhead transcriptional factor (FOXO3a) is a critical effector of the PTEN-mediated tumor suppressor. However, whether the PTEN–Akt–FOXO3a pathway is involved in neuronal apoptosis in developing rat brain after hypoxia–ischemia (HI) is unclear. In this study, we generated an HI model using postnatal day 10 rats. Immunohistochemistry and western blot were used to detect the expression of total and phosphorylated PTEN, Akt, and FOXO3a, as well as its target gene Bim. We found that dephosphorylation of PTEN was accompanied by dephosphorylation of Akt and FOXO3a, which induced FOXO3a translocation into the nucleus and upregulated the expression of Bim. Furthermore, we found that PTEN inhibition by bisperoxovanadium significantly increased the phosphorylation of Akt and FOXO3a, decreased the nuclear translocation of FOXO3a, and inhibited Bim expression after HI. Moreover, the downregulation of Bim caused by PTEN inhibition attenuated cellular apoptosis in developing rat brain. Our findings suggest that the PTEN–Akt–FOXO3a pathway is involved in neuronal apoptosis in neonatal rat brain after HI. Agents targeting PTEN may offer a promise to rescue neurons from HI brain damage.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis Regulatory Proteins - genetics</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Bcl-2-Like Protein 11</subject><subject>Biological and medical sciences</subject><subject>Cell Nucleus - metabolism</subject><subject>Cytoplasm - metabolism</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Female</subject><subject>Forkhead Box Protein O3</subject><subject>Forkhead Transcription Factors - genetics</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>Gene Expression</subject><subject>Hypoxia-Ischemia, Brain - metabolism</subject><subject>Medical sciences</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Neurology</subject><subject>Neurons - cytology</subject><subject>Neuropharmacology</subject><subject>Neuroprotective agent</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphorylation</subject><subject>Protein Transport</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>PTEN Phosphohydrolase - antagonists & inhibitors</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN Phosphohydrolase - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Vanadium Compounds - pharmacology</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0271-678X</issn><issn>1559-7016</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc1uEzEUhS0EoqGwZYlGSMACTfDP-G9TKZSWRlRNhYLU3cjj2ImjmfFgzwSy4x14Q54Eh0QtIMHG1j3-fHyvDwBPERwjSMSbta5sM8YQylTje2CEKJU5h4jdByOIOcoZFzdH4FGMawihIJQ-BEdIMkyQLEZgmLYbX29MY9o-8zbrVya7np9d_fj2ffJhntbz2c2MqOxa9asvapu5NrsyQ_CtqrNJ57veRxd36juzMbXvXLvMPqo-extUEpXtTcgutp3_6lQym0a9Mo1Tj8EDq-ponhz2Y_Dp_Gx-epFfzt5PTyeXuaZc9jkqJOJKLCxcmKTYijNSKVhIuYBMmgpaKirM9aKiQlaWiEJLYQTHkFttKSXH4GTv2w1VYxY6DRlUXXbBNSpsS69c-edJ61bl0m9KLApGqUgGrw4GwX8eTOzLxkVt6lq1xg-x5IQIwongiXz5XxIjjBlmMoHP_wLXfgjpP3eMLAqIGUzQeA_p4GMMxt72jGC5C778FXy5Cz7VOF149vukd_gh6QS8OAAqalXboFrt4i2HMZZUMJS413suqqW5a-0fz_4ESbrIWg</recordid><startdate>20091201</startdate><enddate>20091201</enddate><creator>Li, Deyuan</creator><creator>Qu, Yi</creator><creator>Mao, Meng</creator><creator>Zhang, Xiaolan</creator><creator>Li, Jinhui</creator><creator>Ferriero, Donna</creator><creator>Mu, Dezhi</creator><general>SAGE Publications</general><general>Nature Publishing Group</general><general>Sage Publications Ltd</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7TK</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20091201</creationdate><title>Involvement of the PTEN–AKT–FOXO3a Pathway in Neuronal Apoptosis in Developing Rat Brain after Hypoxia–Ischemia</title><author>Li, Deyuan ; Qu, Yi ; Mao, Meng ; Zhang, Xiaolan ; Li, Jinhui ; Ferriero, Donna ; Mu, Dezhi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c579t-14917a8df0dec57fb763ba0499d069eb0f58b27cdb589bf384c98e87207fcf553</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis Regulatory Proteins - genetics</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Bcl-2-Like Protein 11</topic><topic>Biological and medical sciences</topic><topic>Cell Nucleus - metabolism</topic><topic>Cytoplasm - metabolism</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Female</topic><topic>Forkhead Box Protein O3</topic><topic>Forkhead Transcription Factors - genetics</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>Gene Expression</topic><topic>Hypoxia-Ischemia, Brain - metabolism</topic><topic>Medical sciences</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Neurology</topic><topic>Neurons - cytology</topic><topic>Neuropharmacology</topic><topic>Neuroprotective agent</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphorylation</topic><topic>Protein Transport</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>PTEN Phosphohydrolase - antagonists & inhibitors</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN Phosphohydrolase - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Vanadium Compounds - pharmacology</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Deyuan</creatorcontrib><creatorcontrib>Qu, Yi</creatorcontrib><creatorcontrib>Mao, Meng</creatorcontrib><creatorcontrib>Zhang, Xiaolan</creatorcontrib><creatorcontrib>Li, Jinhui</creatorcontrib><creatorcontrib>Ferriero, Donna</creatorcontrib><creatorcontrib>Mu, Dezhi</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cerebral blood flow and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Deyuan</au><au>Qu, Yi</au><au>Mao, Meng</au><au>Zhang, Xiaolan</au><au>Li, Jinhui</au><au>Ferriero, Donna</au><au>Mu, Dezhi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of the PTEN–AKT–FOXO3a Pathway in Neuronal Apoptosis in Developing Rat Brain after Hypoxia–Ischemia</atitle><jtitle>Journal of cerebral blood flow and metabolism</jtitle><addtitle>J Cereb Blood Flow Metab</addtitle><date>2009-12-01</date><risdate>2009</risdate><volume>29</volume><issue>12</issue><spage>1903</spage><epage>1913</epage><pages>1903-1913</pages><issn>0271-678X</issn><eissn>1559-7016</eissn><coden>JCBMDN</coden><abstract>The proapoptotic function of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) phosphatase has been linked to its capacity to antagonize the phosphatidylinositol-3-kinase–Akt signaling pathway. Previous studies have shown that the Forkhead transcriptional factor (FOXO3a) is a critical effector of the PTEN-mediated tumor suppressor. However, whether the PTEN–Akt–FOXO3a pathway is involved in neuronal apoptosis in developing rat brain after hypoxia–ischemia (HI) is unclear. In this study, we generated an HI model using postnatal day 10 rats. Immunohistochemistry and western blot were used to detect the expression of total and phosphorylated PTEN, Akt, and FOXO3a, as well as its target gene Bim. We found that dephosphorylation of PTEN was accompanied by dephosphorylation of Akt and FOXO3a, which induced FOXO3a translocation into the nucleus and upregulated the expression of Bim. Furthermore, we found that PTEN inhibition by bisperoxovanadium significantly increased the phosphorylation of Akt and FOXO3a, decreased the nuclear translocation of FOXO3a, and inhibited Bim expression after HI. Moreover, the downregulation of Bim caused by PTEN inhibition attenuated cellular apoptosis in developing rat brain. Our findings suggest that the PTEN–Akt–FOXO3a pathway is involved in neuronal apoptosis in neonatal rat brain after HI. Agents targeting PTEN may offer a promise to rescue neurons from HI brain damage.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>19623194</pmid><doi>10.1038/jcbfm.2009.102</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0271-678X |
| ispartof | Journal of cerebral blood flow and metabolism, 2009-12, Vol.29 (12), p.1903-1913 |
| issn | 0271-678X 1559-7016 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2846558 |
| source | SAGE Complete A-Z List; MEDLINE |
| subjects | Animals Apoptosis Apoptosis Regulatory Proteins - genetics Apoptosis Regulatory Proteins - metabolism Bcl-2-Like Protein 11 Biological and medical sciences Cell Nucleus - metabolism Cytoplasm - metabolism Enzyme Inhibitors - pharmacology Female Forkhead Box Protein O3 Forkhead Transcription Factors - genetics Forkhead Transcription Factors - metabolism Gene Expression Hypoxia-Ischemia, Brain - metabolism Medical sciences Membrane Proteins - genetics Membrane Proteins - metabolism Neurology Neurons - cytology Neuropharmacology Neuroprotective agent Pharmacology. Drug treatments Phosphorylation Protein Transport Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism PTEN Phosphohydrolase - antagonists & inhibitors PTEN Phosphohydrolase - genetics PTEN Phosphohydrolase - metabolism Rats Rats, Sprague-Dawley Vanadium Compounds - pharmacology Vascular diseases and vascular malformations of the nervous system |
| title | Involvement of the PTEN–AKT–FOXO3a Pathway in Neuronal Apoptosis in Developing Rat Brain after Hypoxia–Ischemia |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-31T16%3A39%3A15IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Involvement%20of%20the%20PTEN%E2%80%93AKT%E2%80%93FOXO3a%20Pathway%20in%20Neuronal%20Apoptosis%20in%20Developing%20Rat%20Brain%20after%20Hypoxia%E2%80%93Ischemia&rft.jtitle=Journal%20of%20cerebral%20blood%20flow%20and%20metabolism&rft.au=Li,%20Deyuan&rft.date=2009-12-01&rft.volume=29&rft.issue=12&rft.spage=1903&rft.epage=1913&rft.pages=1903-1913&rft.issn=0271-678X&rft.eissn=1559-7016&rft.coden=JCBMDN&rft_id=info:doi/10.1038/jcbfm.2009.102&rft_dat=%3Cproquest_pubme%3E21226269%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=219440260&rft_id=info:pmid/19623194&rft_sage_id=10.1038_jcbfm.2009.102&rfr_iscdi=true |