Plasmalogens rescue neuronal cell death through an activation of AKT and ERK survival signaling
Neuronal cells are susceptible to many stresses, which will cause the apoptosis and neurodegenerative diseases. The precise molecular mechanism behind the neuronal protection against these apoptotic stimuli is necessary for drug discovery. In the present study, we have found that plasmalogens (Pls),...
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| creator | Hossain, Md Shamim Ifuku, Masataka Take, Sachiko Kawamura, Jun Miake, Kiyotaka Katafuchi, Toshihiko |
| description | Neuronal cells are susceptible to many stresses, which will cause the apoptosis and neurodegenerative diseases. The precise molecular mechanism behind the neuronal protection against these apoptotic stimuli is necessary for drug discovery. In the present study, we have found that plasmalogens (Pls), which are glycerophospholipids containing vinyl ether linkage at sn-1 position, can protect the neuronal cell death upon serum deprivation. Interestingly, caspse-9, but not caspase-8 and caspase-12, was cleaved upon the serum starvation in Neuro-2A cells. Pls treatments effectively reduced the activation of caspase-9. Furthermore, cellular signaling experiments showed that Pls enhanced phosphorylation of the phosphoinositide 3-kinase (PI3K)-dependent serine/threonine-specific protein kinase AKT and extracellular-signal-regulated kinases ERK1/2. PI3K/AKT inhibitor LY294002 and MAPK/ERK kinase (MEK) inhibitor U0126 treatments study clearly indicated that Pls-mediated cell survival was dependent on the activation of these kinases. In addition, Pls also inhibited primary mouse hippocampal neuronal cell death induced by nutrient deprivation, which was associated with the inhibition of caspase-9 and caspase-3 cleavages. It was reported that Pls content decreased in the brain of the Alzheimer's patients, which indicated that the reduction of Pls content could endanger neurons. The present findings, taken together, suggest that Pls have an anti-apoptotic action in the brain. Further studies on precise mechanisms of Pls-mediated protection against cell death may lead us to establish a novel therapeutic approach to cure neurodegenerative disorders. |
| doi_str_mv | 10.1371/journal.pone.0083508 |
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The precise molecular mechanism behind the neuronal protection against these apoptotic stimuli is necessary for drug discovery. In the present study, we have found that plasmalogens (Pls), which are glycerophospholipids containing vinyl ether linkage at sn-1 position, can protect the neuronal cell death upon serum deprivation. Interestingly, caspse-9, but not caspase-8 and caspase-12, was cleaved upon the serum starvation in Neuro-2A cells. Pls treatments effectively reduced the activation of caspase-9. Furthermore, cellular signaling experiments showed that Pls enhanced phosphorylation of the phosphoinositide 3-kinase (PI3K)-dependent serine/threonine-specific protein kinase AKT and extracellular-signal-regulated kinases ERK1/2. PI3K/AKT inhibitor LY294002 and MAPK/ERK kinase (MEK) inhibitor U0126 treatments study clearly indicated that Pls-mediated cell survival was dependent on the activation of these kinases. In addition, Pls also inhibited primary mouse hippocampal neuronal cell death induced by nutrient deprivation, which was associated with the inhibition of caspase-9 and caspase-3 cleavages. It was reported that Pls content decreased in the brain of the Alzheimer's patients, which indicated that the reduction of Pls content could endanger neurons. The present findings, taken together, suggest that Pls have an anti-apoptotic action in the brain. Further studies on precise mechanisms of Pls-mediated protection against cell death may lead us to establish a novel therapeutic approach to cure neurodegenerative disorders.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0083508</identifier><identifier>PMID: 24376709</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Alzheimer's disease ; Alzheimers disease ; Animals ; Apoptosis ; Apoptosis - drug effects ; Biochemistry ; Brain ; Brain research ; Caspase ; Caspase-12 ; Caspase-3 ; Caspase-8 ; Caspase-9 ; Caspases - metabolism ; Cell activation ; Cell cycle ; Cell death ; Cell Death - drug effects ; Cell Line, Tumor ; Cell survival ; Cell Survival - drug effects ; Deoxyribonucleic acid ; Deprivation ; DNA ; Enzyme Activation - drug effects ; Enzyme inhibitors ; Enzymes ; Ethanol ; Extracellular signal-regulated kinase ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Hippocampus ; Hippocampus - cytology ; Inhibition ; Inhibitors ; Kinases ; MAP kinase ; Mice ; Mortality ; Nervous system diseases ; Neuroblastoma ; Neurodegenerative diseases ; Neurological diseases ; Neurons ; Neurons - cytology ; Neurons - drug effects ; Neurons - metabolism ; Phosphorylation ; Phosphorylation - drug effects ; Physiology ; Plasmalogens - pharmacology ; Protein kinase ; Protein kinases ; Proteolysis - drug effects ; Proto-Oncogene Proteins c-akt - metabolism ; Signal transduction ; Signal Transduction - drug effects ; Signaling ; Starvation ; Survival ; Threonine ; Tretinoin - pharmacology</subject><ispartof>PloS one, 2013-12, Vol.8 (12), p.e83508-e83508</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Hossain et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://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 Hossain et al 2013 Hossain et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-6c89c118dd5d30cb75a72d53a9b95f4d69cfc8a209643cdc91ca71bc40c32d2a3</citedby><cites>FETCH-LOGICAL-c692t-6c89c118dd5d30cb75a72d53a9b95f4d69cfc8a209643cdc91ca71bc40c32d2a3</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/PMC3869814/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3869814/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,2096,2915,23847,27905,27906,53772,53774,79349,79350</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24376709$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Amin, A R M Ruhul</contributor><creatorcontrib>Hossain, Md Shamim</creatorcontrib><creatorcontrib>Ifuku, Masataka</creatorcontrib><creatorcontrib>Take, Sachiko</creatorcontrib><creatorcontrib>Kawamura, Jun</creatorcontrib><creatorcontrib>Miake, Kiyotaka</creatorcontrib><creatorcontrib>Katafuchi, Toshihiko</creatorcontrib><title>Plasmalogens rescue neuronal cell death through an activation of AKT and ERK survival signaling</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Neuronal cells are susceptible to many stresses, which will cause the apoptosis and neurodegenerative diseases. The precise molecular mechanism behind the neuronal protection against these apoptotic stimuli is necessary for drug discovery. In the present study, we have found that plasmalogens (Pls), which are glycerophospholipids containing vinyl ether linkage at sn-1 position, can protect the neuronal cell death upon serum deprivation. Interestingly, caspse-9, but not caspase-8 and caspase-12, was cleaved upon the serum starvation in Neuro-2A cells. Pls treatments effectively reduced the activation of caspase-9. Furthermore, cellular signaling experiments showed that Pls enhanced phosphorylation of the phosphoinositide 3-kinase (PI3K)-dependent serine/threonine-specific protein kinase AKT and extracellular-signal-regulated kinases ERK1/2. PI3K/AKT inhibitor LY294002 and MAPK/ERK kinase (MEK) inhibitor U0126 treatments study clearly indicated that Pls-mediated cell survival was dependent on the activation of these kinases. In addition, Pls also inhibited primary mouse hippocampal neuronal cell death induced by nutrient deprivation, which was associated with the inhibition of caspase-9 and caspase-3 cleavages. It was reported that Pls content decreased in the brain of the Alzheimer's patients, which indicated that the reduction of Pls content could endanger neurons. The present findings, taken together, suggest that Pls have an anti-apoptotic action in the brain. Further studies on precise mechanisms of Pls-mediated protection against cell death may lead us to establish a novel therapeutic approach to cure neurodegenerative disorders.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Alzheimer's disease</subject><subject>Alzheimers disease</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biochemistry</subject><subject>Brain</subject><subject>Brain research</subject><subject>Caspase</subject><subject>Caspase-12</subject><subject>Caspase-3</subject><subject>Caspase-8</subject><subject>Caspase-9</subject><subject>Caspases - metabolism</subject><subject>Cell activation</subject><subject>Cell cycle</subject><subject>Cell death</subject><subject>Cell Death - drug effects</subject><subject>Cell Line, Tumor</subject><subject>Cell survival</subject><subject>Cell Survival - drug effects</subject><subject>Deoxyribonucleic acid</subject><subject>Deprivation</subject><subject>DNA</subject><subject>Enzyme Activation - drug effects</subject><subject>Enzyme inhibitors</subject><subject>Enzymes</subject><subject>Ethanol</subject><subject>Extracellular signal-regulated kinase</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Hippocampus</subject><subject>Hippocampus - cytology</subject><subject>Inhibition</subject><subject>Inhibitors</subject><subject>Kinases</subject><subject>MAP kinase</subject><subject>Mice</subject><subject>Mortality</subject><subject>Nervous system diseases</subject><subject>Neuroblastoma</subject><subject>Neurodegenerative diseases</subject><subject>Neurological diseases</subject><subject>Neurons</subject><subject>Neurons - cytology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Physiology</subject><subject>Plasmalogens - pharmacology</subject><subject>Protein kinase</subject><subject>Protein kinases</subject><subject>Proteolysis - drug effects</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><subject>Starvation</subject><subject>Survival</subject><subject>Threonine</subject><subject>Tretinoin - pharmacology</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>eNqNk12L1DAUhoso7rr6D0QDgujFjPlqm9wIw7LqsAsr6-ptSJO0zZBpxqQd9N-bOt1lKnshvUg5ed73JCfnZNlLBJeIlOjDxg-hk265851ZQshIDtmj7BRxghcFhuTx0f9J9izGDYQ5YUXxNDvBlJRFCflpJr46GbfS-cZ0EQQT1WBAZ4bgkzdQxjmgjexb0LfBD00LZAek6u1e9tZ3wNdgdXmbghpc3FyCOIR92nIg2ibpbdc8z57U0kXzYlrPsu-fLm7Pvyyurj-vz1dXC1Vw3C8KxbhCiGmdawJVVeayxDonklc8r6kuuKoVkxjyghKlFUdKlqhSFCqCNZbkLHt98N05H8VUmygQLSEsOYIoEesDob3ciF2wWxl-Cy-t-BvwoREy9FY5I1hhIEtpa6pqSnXNOWaaYpMrU1Atq-T1cco2VFujlen6IN3MdL7T2VY0fi9S_TlDNBm8mwyC_zmY2IutjWO1ZWf8MJ6bwxJhQnFC3_yDPny7iWpkuoDtap_yqtFUrGjJMKSYjWmXD1Dp02ZrVWqk2qb4TPB-JkhMb371jRxiFOtvN__PXv-Ys2-P2NZI17fRu2FsqjgH6QFUwccYTH1fZATFOAd31RDjHIhpDpLs1fED3YvuGp_8AazIAxY</recordid><startdate>20131220</startdate><enddate>20131220</enddate><creator>Hossain, Md Shamim</creator><creator>Ifuku, Masataka</creator><creator>Take, Sachiko</creator><creator>Kawamura, Jun</creator><creator>Miake, Kiyotaka</creator><creator>Katafuchi, Toshihiko</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>AEUYN</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>20131220</creationdate><title>Plasmalogens rescue neuronal cell death through an activation of AKT and ERK survival signaling</title><author>Hossain, Md Shamim ; Ifuku, Masataka ; Take, Sachiko ; Kawamura, Jun ; Miake, Kiyotaka ; Katafuchi, Toshihiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-6c89c118dd5d30cb75a72d53a9b95f4d69cfc8a209643cdc91ca71bc40c32d2a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Alzheimer's disease</topic><topic>Alzheimers disease</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - 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The precise molecular mechanism behind the neuronal protection against these apoptotic stimuli is necessary for drug discovery. In the present study, we have found that plasmalogens (Pls), which are glycerophospholipids containing vinyl ether linkage at sn-1 position, can protect the neuronal cell death upon serum deprivation. Interestingly, caspse-9, but not caspase-8 and caspase-12, was cleaved upon the serum starvation in Neuro-2A cells. Pls treatments effectively reduced the activation of caspase-9. Furthermore, cellular signaling experiments showed that Pls enhanced phosphorylation of the phosphoinositide 3-kinase (PI3K)-dependent serine/threonine-specific protein kinase AKT and extracellular-signal-regulated kinases ERK1/2. PI3K/AKT inhibitor LY294002 and MAPK/ERK kinase (MEK) inhibitor U0126 treatments study clearly indicated that Pls-mediated cell survival was dependent on the activation of these kinases. In addition, Pls also inhibited primary mouse hippocampal neuronal cell death induced by nutrient deprivation, which was associated with the inhibition of caspase-9 and caspase-3 cleavages. It was reported that Pls content decreased in the brain of the Alzheimer's patients, which indicated that the reduction of Pls content could endanger neurons. The present findings, taken together, suggest that Pls have an anti-apoptotic action in the brain. Further studies on precise mechanisms of Pls-mediated protection against cell death may lead us to establish a novel therapeutic approach to cure neurodegenerative disorders.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24376709</pmid><doi>10.1371/journal.pone.0083508</doi><tpages>e83508</tpages><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1470079101 |
| 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 Alzheimer's disease Alzheimers disease Animals Apoptosis Apoptosis - drug effects Biochemistry Brain Brain research Caspase Caspase-12 Caspase-3 Caspase-8 Caspase-9 Caspases - metabolism Cell activation Cell cycle Cell death Cell Death - drug effects Cell Line, Tumor Cell survival Cell Survival - drug effects Deoxyribonucleic acid Deprivation DNA Enzyme Activation - drug effects Enzyme inhibitors Enzymes Ethanol Extracellular signal-regulated kinase Extracellular Signal-Regulated MAP Kinases - metabolism Hippocampus Hippocampus - cytology Inhibition Inhibitors Kinases MAP kinase Mice Mortality Nervous system diseases Neuroblastoma Neurodegenerative diseases Neurological diseases Neurons Neurons - cytology Neurons - drug effects Neurons - metabolism Phosphorylation Phosphorylation - drug effects Physiology Plasmalogens - pharmacology Protein kinase Protein kinases Proteolysis - drug effects Proto-Oncogene Proteins c-akt - metabolism Signal transduction Signal Transduction - drug effects Signaling Starvation Survival Threonine Tretinoin - pharmacology |
| title | Plasmalogens rescue neuronal cell death through an activation of AKT and ERK survival signaling |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-21T06%3A15%3A52IST&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=Plasmalogens%20rescue%20neuronal%20cell%20death%20through%20an%20activation%20of%20AKT%20and%20ERK%20survival%20signaling&rft.jtitle=PloS%20one&rft.au=Hossain,%20Md%20Shamim&rft.date=2013-12-20&rft.volume=8&rft.issue=12&rft.spage=e83508&rft.epage=e83508&rft.pages=e83508-e83508&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0083508&rft_dat=%3Cgale_plos_%3EA478204284%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=1470079101&rft_id=info:pmid/24376709&rft_galeid=A478204284&rft_doaj_id=oai_doaj_org_article_86e085f4f4cf44df9928d42e5ce64dab&rfr_iscdi=true |