Effects of bone marrow-derived mesenchymal stem cells on the axonal outgrowth through activation of PI3K/AKT signaling in primary cortical neurons followed oxygen-glucose deprivation injury
Transplantation with bone marrow-derived mesenchymal stem cells (BMSCs) improves the survival of neurons and axonal outgrowth after stroke remains undetermined. Here, we investigated whether PI3K/AKT signaling pathway is involved in these therapeutic effects of BMSCs. (1) BMSCs and cortical neurons...
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| Veröffentlicht in: | PloS one 2013-11, Vol.8 (11), p.e78514-e78514 |
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| creator | Liu, Yong Zhang, Yixian Lin, Longzai Lin, Feifei Li, Tin Du, Houwei Chen, Ronghua Zheng, Wei Liu, Nan |
| description | Transplantation with bone marrow-derived mesenchymal stem cells (BMSCs) improves the survival of neurons and axonal outgrowth after stroke remains undetermined. Here, we investigated whether PI3K/AKT signaling pathway is involved in these therapeutic effects of BMSCs.
(1) BMSCs and cortical neurons were derived from Sprague-Dawley rats. The injured neurons were induced by Oxygen-Glucose Deprivation (OGD), and then were respectively co-cultured for 48 hours with BMSCs at different densities (5×10(3), 5×10(5)/ml) in transwell co-culture system. The average length of axon and expression of GAP-43 were examined to assess the effect of BMSCs on axonal outgrowth after the damage of neurons induced by OGD. (2) The injured neurons were cultured with a conditioned medium (CM) of BMSCs cultured for 24 hours in neurobasal medium. During the process, we further identified whether PI3K/AKT signaling pathway is involved through the adjunction of LY294002 (a specific phosphatidylinositide-3-kinase (PI3K) inhibitor). Two hours later, the expression of pAKT (phosphorylated AKT) and AKT were analyzed by Western blotting. The length of axons, the expression of GAP-43 and the survival of neurons were measured at 48 hours.
Both BMSCs and CM from BMSCs inreased the axonal length and GAP-43 expression in OGD-injured cortical neurons. There was no difference between the effects of BMSCs of 5×10(5)/ml and of 5×10(3)/ml on axonal outgrowth. Expression of pAKT enhanced significantly at 2 hours and the neuron survival increased at 48 hours after the injured neurons cultured with the CM, respectively. These effects of CM were prevented by inhibitor LY294002.
BMSCs promote axonal outgrowth and the survival of neurons against the damage from OGD in vitro by the paracrine effects through PI3K/AKT signaling pathway. |
| doi_str_mv | 10.1371/journal.pone.0078514 |
| format | Article |
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(1) BMSCs and cortical neurons were derived from Sprague-Dawley rats. The injured neurons were induced by Oxygen-Glucose Deprivation (OGD), and then were respectively co-cultured for 48 hours with BMSCs at different densities (5×10(3), 5×10(5)/ml) in transwell co-culture system. The average length of axon and expression of GAP-43 were examined to assess the effect of BMSCs on axonal outgrowth after the damage of neurons induced by OGD. (2) The injured neurons were cultured with a conditioned medium (CM) of BMSCs cultured for 24 hours in neurobasal medium. During the process, we further identified whether PI3K/AKT signaling pathway is involved through the adjunction of LY294002 (a specific phosphatidylinositide-3-kinase (PI3K) inhibitor). Two hours later, the expression of pAKT (phosphorylated AKT) and AKT were analyzed by Western blotting. The length of axons, the expression of GAP-43 and the survival of neurons were measured at 48 hours.
Both BMSCs and CM from BMSCs inreased the axonal length and GAP-43 expression in OGD-injured cortical neurons. There was no difference between the effects of BMSCs of 5×10(5)/ml and of 5×10(3)/ml on axonal outgrowth. Expression of pAKT enhanced significantly at 2 hours and the neuron survival increased at 48 hours after the injured neurons cultured with the CM, respectively. These effects of CM were prevented by inhibitor LY294002.
BMSCs promote axonal outgrowth and the survival of neurons against the damage from OGD in vitro by the paracrine effects through PI3K/AKT signaling pathway.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0078514</identifier><identifier>PMID: 24265694</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Analysis ; Animals ; Axons ; Axons - metabolism ; Bone marrow ; Bone Marrow Cells - cytology ; Bone marrow transplantation ; Brain - cytology ; Brain research ; Cell culture ; Cell cycle ; Cell Survival ; Conditioning ; Damage assessment ; Deprivation ; Enzyme inhibitors ; Female ; GAP-43 protein ; GAP-43 Protein - metabolism ; Gene Expression Regulation ; Glucose ; Glucose - deficiency ; Health aspects ; Inhibitors ; Injuries ; Insulin-like growth factors ; Ischemia ; Kinases ; Laboratory animals ; Mesenchymal Stem Cell Transplantation ; Mesenchymal stem cells ; Mesenchymal Stromal Cells - cytology ; Mesenchyme ; Neurogenesis ; Neurology ; Neurons ; Oxygen ; Oxygen - metabolism ; Paracrine signalling ; Phosphatidylinositol 3-Kinases - metabolism ; Pregnancy ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Sprague-Dawley ; Rodents ; Signal Transduction ; Stem cells ; Stroke ; Survival ; Transplantation ; Transplants & implants ; Western blotting</subject><ispartof>PloS one, 2013-11, Vol.8 (11), p.e78514-e78514</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Liu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Liu et al 2013 Liu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-39786b2f820083f26673f0e23d6f850abcc66b51ca8de85d63b23a8af5a5ffb83</citedby><cites>FETCH-LOGICAL-c758t-39786b2f820083f26673f0e23d6f850abcc66b51ca8de85d63b23a8af5a5ffb83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3827028/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3827028/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24265694$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Karamyan, Vardan</contributor><creatorcontrib>Liu, Yong</creatorcontrib><creatorcontrib>Zhang, Yixian</creatorcontrib><creatorcontrib>Lin, Longzai</creatorcontrib><creatorcontrib>Lin, Feifei</creatorcontrib><creatorcontrib>Li, Tin</creatorcontrib><creatorcontrib>Du, Houwei</creatorcontrib><creatorcontrib>Chen, Ronghua</creatorcontrib><creatorcontrib>Zheng, Wei</creatorcontrib><creatorcontrib>Liu, Nan</creatorcontrib><title>Effects of bone marrow-derived mesenchymal stem cells on the axonal outgrowth through activation of PI3K/AKT signaling in primary cortical neurons followed oxygen-glucose deprivation injury</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Transplantation with bone marrow-derived mesenchymal stem cells (BMSCs) improves the survival of neurons and axonal outgrowth after stroke remains undetermined. Here, we investigated whether PI3K/AKT signaling pathway is involved in these therapeutic effects of BMSCs.
(1) BMSCs and cortical neurons were derived from Sprague-Dawley rats. The injured neurons were induced by Oxygen-Glucose Deprivation (OGD), and then were respectively co-cultured for 48 hours with BMSCs at different densities (5×10(3), 5×10(5)/ml) in transwell co-culture system. The average length of axon and expression of GAP-43 were examined to assess the effect of BMSCs on axonal outgrowth after the damage of neurons induced by OGD. (2) The injured neurons were cultured with a conditioned medium (CM) of BMSCs cultured for 24 hours in neurobasal medium. During the process, we further identified whether PI3K/AKT signaling pathway is involved through the adjunction of LY294002 (a specific phosphatidylinositide-3-kinase (PI3K) inhibitor). Two hours later, the expression of pAKT (phosphorylated AKT) and AKT were analyzed by Western blotting. The length of axons, the expression of GAP-43 and the survival of neurons were measured at 48 hours.
Both BMSCs and CM from BMSCs inreased the axonal length and GAP-43 expression in OGD-injured cortical neurons. There was no difference between the effects of BMSCs of 5×10(5)/ml and of 5×10(3)/ml on axonal outgrowth. Expression of pAKT enhanced significantly at 2 hours and the neuron survival increased at 48 hours after the injured neurons cultured with the CM, respectively. These effects of CM were prevented by inhibitor LY294002.
BMSCs promote axonal outgrowth and the survival of neurons against the damage from OGD in vitro by the paracrine effects through PI3K/AKT signaling pathway.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Analysis</subject><subject>Animals</subject><subject>Axons</subject><subject>Axons - metabolism</subject><subject>Bone marrow</subject><subject>Bone Marrow Cells - cytology</subject><subject>Bone marrow transplantation</subject><subject>Brain - cytology</subject><subject>Brain research</subject><subject>Cell culture</subject><subject>Cell cycle</subject><subject>Cell Survival</subject><subject>Conditioning</subject><subject>Damage assessment</subject><subject>Deprivation</subject><subject>Enzyme inhibitors</subject><subject>Female</subject><subject>GAP-43 protein</subject><subject>GAP-43 Protein - metabolism</subject><subject>Gene Expression Regulation</subject><subject>Glucose</subject><subject>Glucose - deficiency</subject><subject>Health aspects</subject><subject>Inhibitors</subject><subject>Injuries</subject><subject>Insulin-like growth factors</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Mesenchymal Stem Cell Transplantation</subject><subject>Mesenchymal stem cells</subject><subject>Mesenchymal Stromal Cells - cytology</subject><subject>Mesenchyme</subject><subject>Neurogenesis</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Oxygen</subject><subject>Oxygen - metabolism</subject><subject>Paracrine signalling</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Pregnancy</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Stem cells</subject><subject>Stroke</subject><subject>Survival</subject><subject>Transplantation</subject><subject>Transplants & implants</subject><subject>Western blotting</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk8tu1DAUhiMEolB4AwSWkBAsZupL7Hg2SFVVYNRKRVDYWo5jJx4ldrGdtvNwvBsOTasO6gJlkejk-_9zsU9RvEJwiUiFDjZ-DE72ywvv9BLCilNUPiqeoRXBC4YheXzve694HuMGQko4Y0-LPVxiRtmqfFb8PjZGqxSBN6DOTmCQIfirRaODvdQNGHTUTnXbQfYgJj0Apfs-0w6kTgN57XMJwI-pzaLU5WDwY9sBqZK9lMlmLht_XZOTg8OTcxBtm3nrWmAduAg2J9sC5UOyKts4PQbvIjC-7_1VTu6vt612i7YflY8aNDpLZlfrNmPYviieGNlH_XJ-7xc_Ph2fH31ZnJ59Xh8dni5URXlakFXFWY0NxxByYjBjFTFQY9IwwymUtVKM1RQpyRvNacNIjYnk0lBJjak52S_e3Phe9D6KefJRoJJCXHJUrjKxviEaLzdibk14acXfgA-tkFObvRao4ZCwimtIqzJnXFVUcVOiskYQUYmz18c521gPulHapSD7HdPdP852ovWXgnBcQTyV-342CP7XqGMSg43TwUmn_TjVzRCvOC5ZRt_-gz7c3Uy1MjdgnfE5r5pMxWFZcZLHSidq-QCVn0YPVuXLZWyO7wg-7Agyk_R1auUYo1h___b_7NnPXfbdPbbTsk9d9P043Zy4C5Y3oAo-xqDN3ZARFNOW3U5DTFsm5i3Lstf3D-hOdLtW5A9WMSY5</recordid><startdate>20131112</startdate><enddate>20131112</enddate><creator>Liu, Yong</creator><creator>Zhang, Yixian</creator><creator>Lin, Longzai</creator><creator>Lin, Feifei</creator><creator>Li, Tin</creator><creator>Du, Houwei</creator><creator>Chen, Ronghua</creator><creator>Zheng, Wei</creator><creator>Liu, Nan</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20131112</creationdate><title>Effects of bone marrow-derived mesenchymal stem cells on the axonal outgrowth through activation of PI3K/AKT signaling in primary cortical neurons followed oxygen-glucose deprivation injury</title><author>Liu, Yong ; Zhang, Yixian ; Lin, Longzai ; Lin, Feifei ; Li, Tin ; Du, Houwei ; Chen, Ronghua ; Zheng, Wei ; Liu, Nan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-39786b2f820083f26673f0e23d6f850abcc66b51ca8de85d63b23a8af5a5ffb83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Analysis</topic><topic>Animals</topic><topic>Axons</topic><topic>Axons - metabolism</topic><topic>Bone marrow</topic><topic>Bone Marrow Cells - cytology</topic><topic>Bone marrow transplantation</topic><topic>Brain - cytology</topic><topic>Brain research</topic><topic>Cell culture</topic><topic>Cell cycle</topic><topic>Cell Survival</topic><topic>Conditioning</topic><topic>Damage assessment</topic><topic>Deprivation</topic><topic>Enzyme inhibitors</topic><topic>Female</topic><topic>GAP-43 protein</topic><topic>GAP-43 Protein - metabolism</topic><topic>Gene Expression Regulation</topic><topic>Glucose</topic><topic>Glucose - deficiency</topic><topic>Health aspects</topic><topic>Inhibitors</topic><topic>Injuries</topic><topic>Insulin-like growth factors</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Mesenchymal Stem Cell Transplantation</topic><topic>Mesenchymal stem cells</topic><topic>Mesenchymal Stromal Cells - cytology</topic><topic>Mesenchyme</topic><topic>Neurogenesis</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Oxygen</topic><topic>Oxygen - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Yong</au><au>Zhang, Yixian</au><au>Lin, Longzai</au><au>Lin, Feifei</au><au>Li, Tin</au><au>Du, Houwei</au><au>Chen, Ronghua</au><au>Zheng, Wei</au><au>Liu, Nan</au><au>Karamyan, Vardan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of bone marrow-derived mesenchymal stem cells on the axonal outgrowth through activation of PI3K/AKT signaling in primary cortical neurons followed oxygen-glucose deprivation injury</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-11-12</date><risdate>2013</risdate><volume>8</volume><issue>11</issue><spage>e78514</spage><epage>e78514</epage><pages>e78514-e78514</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Transplantation with bone marrow-derived mesenchymal stem cells (BMSCs) improves the survival of neurons and axonal outgrowth after stroke remains undetermined. Here, we investigated whether PI3K/AKT signaling pathway is involved in these therapeutic effects of BMSCs.
(1) BMSCs and cortical neurons were derived from Sprague-Dawley rats. The injured neurons were induced by Oxygen-Glucose Deprivation (OGD), and then were respectively co-cultured for 48 hours with BMSCs at different densities (5×10(3), 5×10(5)/ml) in transwell co-culture system. The average length of axon and expression of GAP-43 were examined to assess the effect of BMSCs on axonal outgrowth after the damage of neurons induced by OGD. (2) The injured neurons were cultured with a conditioned medium (CM) of BMSCs cultured for 24 hours in neurobasal medium. During the process, we further identified whether PI3K/AKT signaling pathway is involved through the adjunction of LY294002 (a specific phosphatidylinositide-3-kinase (PI3K) inhibitor). Two hours later, the expression of pAKT (phosphorylated AKT) and AKT were analyzed by Western blotting. The length of axons, the expression of GAP-43 and the survival of neurons were measured at 48 hours.
Both BMSCs and CM from BMSCs inreased the axonal length and GAP-43 expression in OGD-injured cortical neurons. There was no difference between the effects of BMSCs of 5×10(5)/ml and of 5×10(3)/ml on axonal outgrowth. Expression of pAKT enhanced significantly at 2 hours and the neuron survival increased at 48 hours after the injured neurons cultured with the CM, respectively. These effects of CM were prevented by inhibitor LY294002.
BMSCs promote axonal outgrowth and the survival of neurons against the damage from OGD in vitro by the paracrine effects through PI3K/AKT signaling pathway.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24265694</pmid><doi>10.1371/journal.pone.0078514</doi><tpages>e78514</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2013-11, Vol.8 (11), p.e78514-e78514 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1450248149 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Analysis Animals Axons Axons - metabolism Bone marrow Bone Marrow Cells - cytology Bone marrow transplantation Brain - cytology Brain research Cell culture Cell cycle Cell Survival Conditioning Damage assessment Deprivation Enzyme inhibitors Female GAP-43 protein GAP-43 Protein - metabolism Gene Expression Regulation Glucose Glucose - deficiency Health aspects Inhibitors Injuries Insulin-like growth factors Ischemia Kinases Laboratory animals Mesenchymal Stem Cell Transplantation Mesenchymal stem cells Mesenchymal Stromal Cells - cytology Mesenchyme Neurogenesis Neurology Neurons Oxygen Oxygen - metabolism Paracrine signalling Phosphatidylinositol 3-Kinases - metabolism Pregnancy Proteins Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Sprague-Dawley Rodents Signal Transduction Stem cells Stroke Survival Transplantation Transplants & implants Western blotting |
| title | Effects of bone marrow-derived mesenchymal stem cells on the axonal outgrowth through activation of PI3K/AKT signaling in primary cortical neurons followed oxygen-glucose deprivation injury |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-05T05%3A32%3A32IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Effects%20of%20bone%20marrow-derived%20mesenchymal%20stem%20cells%20on%20the%20axonal%20outgrowth%20through%20activation%20of%20PI3K/AKT%20signaling%20in%20primary%20cortical%20neurons%20followed%20oxygen-glucose%20deprivation%20injury&rft.jtitle=PloS%20one&rft.au=Liu,%20Yong&rft.date=2013-11-12&rft.volume=8&rft.issue=11&rft.spage=e78514&rft.epage=e78514&rft.pages=e78514-e78514&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0078514&rft_dat=%3Cgale_plos_%3EA478300859%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1450248149&rft_id=info:pmid/24265694&rft_galeid=A478300859&rft_doaj_id=oai_doaj_org_article_1d803678e0574a8d975c8f414b1015a2&rfr_iscdi=true |