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Calcium-dependent cytosolic phospholipase A2 activation is implicated in neuroinflammation and oxidative stress associated with ApoE4

Background Apolipoprotein E4 (APOE4) is associated with a greater response to neuroinflammation and the risk of developing late-onset Alzheimer's disease (AD), but the mechanisms for this association are not clear. The activation of calcium-dependent cytosolic phospholipase A.sub.2 (cPLA2) is i...

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Published in:Molecular neurodegeneration 2022-06, Vol.17 (1), p.1-21, Article 42
Main Authors: Wang, Shaowei, Li, Boyang, Solomon, Victoria, Fonteh, Alfred, Rapoport, Stanley I, Bennett, David A, Arvanitakis, Zoe, Chui, Helena C, Sullivan, Patrick M, Yassine, Hussein N
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creator Wang, Shaowei
Li, Boyang
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Rapoport, Stanley I
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Sullivan, Patrick M
Yassine, Hussein N
description Background Apolipoprotein E4 (APOE4) is associated with a greater response to neuroinflammation and the risk of developing late-onset Alzheimer's disease (AD), but the mechanisms for this association are not clear. The activation of calcium-dependent cytosolic phospholipase A.sub.2 (cPLA2) is involved in inflammatory signaling and is elevated within the plaques of AD brains. The relation between APOE4 genotype and cPLA2 activity is not known. Methods Mouse primary astrocytes, mouse and human brain samples differing by APOE genotypes were collected for measuring cPLA2 expression, phosphorylation, and activity in relation to measures of inflammation and oxidative stress. Results Greater cPLA2 phosphorylation, cPLA2 activity and leukotriene B4 (LTB4) levels were identified in ApoE4 compared to ApoE3 in primary astrocytes, brains of ApoE-targeted replacement (ApoE-TR) mice, and in human brain homogenates from the inferior frontal cortex of persons with AD dementia carrying APOE3/4 compared to APOE3/3. Higher phosphorylated p38 MAPK but not ERK1/2 was found in ApoE4 primary astrocytes and mouse brains than that in ApoE3. Greater cPLA2 translocation to cytosol was observed in human postmortem frontal cortical synaptosomes with recombinant ApoE4 than ApoE3 ex vivo. In ApoE4 astrocytes, the greater levels of LTB4, reactive oxygen species (ROS), and inducible nitric oxide synthase (iNOS) were reduced after cPLA2 inhibition. Conclusions Our findings implicate greater activation of cPLA2 signaling system with APOE4, which could represent a potential drug target for mitigating the increased neuroinflammation with APOE4 and AD. Keywords: cPLA2, ApoE4, Alzheimer's disease, p38 MAPK, Neuroinflammation, Oxidative stress
doi_str_mv 10.1186/s13024-022-00549-5
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The activation of calcium-dependent cytosolic phospholipase A.sub.2 (cPLA2) is involved in inflammatory signaling and is elevated within the plaques of AD brains. The relation between APOE4 genotype and cPLA2 activity is not known. Methods Mouse primary astrocytes, mouse and human brain samples differing by APOE genotypes were collected for measuring cPLA2 expression, phosphorylation, and activity in relation to measures of inflammation and oxidative stress. Results Greater cPLA2 phosphorylation, cPLA2 activity and leukotriene B4 (LTB4) levels were identified in ApoE4 compared to ApoE3 in primary astrocytes, brains of ApoE-targeted replacement (ApoE-TR) mice, and in human brain homogenates from the inferior frontal cortex of persons with AD dementia carrying APOE3/4 compared to APOE3/3. Higher phosphorylated p38 MAPK but not ERK1/2 was found in ApoE4 primary astrocytes and mouse brains than that in ApoE3. Greater cPLA2 translocation to cytosol was observed in human postmortem frontal cortical synaptosomes with recombinant ApoE4 than ApoE3 ex vivo. In ApoE4 astrocytes, the greater levels of LTB4, reactive oxygen species (ROS), and inducible nitric oxide synthase (iNOS) were reduced after cPLA2 inhibition. Conclusions Our findings implicate greater activation of cPLA2 signaling system with APOE4, which could represent a potential drug target for mitigating the increased neuroinflammation with APOE4 and AD. Keywords: cPLA2, ApoE4, Alzheimer's disease, p38 MAPK, Neuroinflammation, Oxidative stress</description><identifier>ISSN: 1750-1326</identifier><identifier>EISSN: 1750-1326</identifier><identifier>DOI: 10.1186/s13024-022-00549-5</identifier><identifier>PMID: 35705959</identifier><language>eng</language><publisher>London: BioMed Central Ltd</publisher><subject>Advertising executives ; Alzheimer's disease ; Antibodies ; ApoE4 ; Apolipoprotein E ; Apolipoprotein E4 ; Apolipoproteins ; Astrocytes ; Brain ; Calcium ; Cortex (frontal) ; cPLA2 ; Cyclin-dependent kinases ; Cytosol ; Dementia ; Dementia disorders ; Development and progression ; Enzymes ; Fatty acids ; Genotypes ; Inflammation ; Kinases ; Leukotriene B4 ; MAP kinase ; Metabolism ; Neurodegenerative diseases ; Neuroinflammation ; Nitric oxide ; Nitric-oxide synthase ; Oxidative stress ; p38 MAPK ; Phospholipase A2 ; Phospholipases ; Phosphorylation ; Plaques ; Proteins ; Reactive oxygen species ; Synaptosomes ; Target marketing ; Therapeutic targets</subject><ispartof>Molecular neurodegeneration, 2022-06, Vol.17 (1), p.1-21, Article 42</ispartof><rights>COPYRIGHT 2022 BioMed Central Ltd.</rights><rights>2022. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022. The Author(s).</rights><rights>The Author(s) 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4555-d6c586413404d795cfb271d5a29eb6f676542ba415b90336d9d2799659ecc3243</citedby><cites>FETCH-LOGICAL-c4555-d6c586413404d795cfb271d5a29eb6f676542ba415b90336d9d2799659ecc3243</cites><orcidid>0000-0002-2483-649X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9202185/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2678218672?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793</link.rule.ids></links><search><creatorcontrib>Wang, Shaowei</creatorcontrib><creatorcontrib>Li, Boyang</creatorcontrib><creatorcontrib>Solomon, Victoria</creatorcontrib><creatorcontrib>Fonteh, Alfred</creatorcontrib><creatorcontrib>Rapoport, Stanley I</creatorcontrib><creatorcontrib>Bennett, David A</creatorcontrib><creatorcontrib>Arvanitakis, Zoe</creatorcontrib><creatorcontrib>Chui, Helena C</creatorcontrib><creatorcontrib>Sullivan, Patrick M</creatorcontrib><creatorcontrib>Yassine, Hussein N</creatorcontrib><title>Calcium-dependent cytosolic phospholipase A2 activation is implicated in neuroinflammation and oxidative stress associated with ApoE4</title><title>Molecular neurodegeneration</title><description>Background Apolipoprotein E4 (APOE4) is associated with a greater response to neuroinflammation and the risk of developing late-onset Alzheimer's disease (AD), but the mechanisms for this association are not clear. The activation of calcium-dependent cytosolic phospholipase A.sub.2 (cPLA2) is involved in inflammatory signaling and is elevated within the plaques of AD brains. The relation between APOE4 genotype and cPLA2 activity is not known. Methods Mouse primary astrocytes, mouse and human brain samples differing by APOE genotypes were collected for measuring cPLA2 expression, phosphorylation, and activity in relation to measures of inflammation and oxidative stress. Results Greater cPLA2 phosphorylation, cPLA2 activity and leukotriene B4 (LTB4) levels were identified in ApoE4 compared to ApoE3 in primary astrocytes, brains of ApoE-targeted replacement (ApoE-TR) mice, and in human brain homogenates from the inferior frontal cortex of persons with AD dementia carrying APOE3/4 compared to APOE3/3. Higher phosphorylated p38 MAPK but not ERK1/2 was found in ApoE4 primary astrocytes and mouse brains than that in ApoE3. Greater cPLA2 translocation to cytosol was observed in human postmortem frontal cortical synaptosomes with recombinant ApoE4 than ApoE3 ex vivo. In ApoE4 astrocytes, the greater levels of LTB4, reactive oxygen species (ROS), and inducible nitric oxide synthase (iNOS) were reduced after cPLA2 inhibition. Conclusions Our findings implicate greater activation of cPLA2 signaling system with APOE4, which could represent a potential drug target for mitigating the increased neuroinflammation with APOE4 and AD. Keywords: cPLA2, ApoE4, Alzheimer's disease, p38 MAPK, Neuroinflammation, Oxidative stress</description><subject>Advertising executives</subject><subject>Alzheimer's disease</subject><subject>Antibodies</subject><subject>ApoE4</subject><subject>Apolipoprotein E</subject><subject>Apolipoprotein E4</subject><subject>Apolipoproteins</subject><subject>Astrocytes</subject><subject>Brain</subject><subject>Calcium</subject><subject>Cortex (frontal)</subject><subject>cPLA2</subject><subject>Cyclin-dependent kinases</subject><subject>Cytosol</subject><subject>Dementia</subject><subject>Dementia disorders</subject><subject>Development and progression</subject><subject>Enzymes</subject><subject>Fatty acids</subject><subject>Genotypes</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Leukotriene B4</subject><subject>MAP kinase</subject><subject>Metabolism</subject><subject>Neurodegenerative diseases</subject><subject>Neuroinflammation</subject><subject>Nitric oxide</subject><subject>Nitric-oxide synthase</subject><subject>Oxidative stress</subject><subject>p38 MAPK</subject><subject>Phospholipase A2</subject><subject>Phospholipases</subject><subject>Phosphorylation</subject><subject>Plaques</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Synaptosomes</subject><subject>Target marketing</subject><subject>Therapeutic targets</subject><issn>1750-1326</issn><issn>1750-1326</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptksuOFCEUQCtG4zz0B1yRuHFTI1A8io1JpzPqJJO40TWh4VY3nSoooap1PsD_luqejLYxhPA695ALt6reEHxDSCveZ9JgympMaY0xZ6rmz6pLIjmuSUPF87_mF9VVznuMmSzgy-qi4RJzxdVl9WtteuvnoXYwQnAQJmQfpphj7y0adzGX3vvRZEArioyd_MFMPgbkM_LDWCgzgUM-oABzij50vRmGE2KCQ_Gnd2V1AJSnBDkjk3O0_hj0w087tBrjLXtVvehMn-H143hdfft4-3X9ub7_8uluvbqvLeOc105Y3gpGGoaZk4rbbkMlcdxQBRvRCSk4oxvDCN8o3DTCKUelUoIrsLahrLmu7k5eF81ej8kPJj3oaLw-bsS01SZN3vagVREWf9dSA4wL0WKJnVHEgQRnJC-uDyfXOG8GcLY8XTL9mfT8JPid3saDVhRT0i6Cd4-CFL_PkCc9-Gyh702AOGdNhZRcMqJIQd_-g-7jnEJ5qoVqi05I-ofampJA-YpY7rWLVK8kbhuOSbtQN_-hSnMweBsDdL7snwXQU4BNMecE3VOOBOulEPWpEHUpRH0sRM2b37hTz-g</recordid><startdate>20220615</startdate><enddate>20220615</enddate><creator>Wang, Shaowei</creator><creator>Li, Boyang</creator><creator>Solomon, Victoria</creator><creator>Fonteh, Alfred</creator><creator>Rapoport, Stanley I</creator><creator>Bennett, David A</creator><creator>Arvanitakis, Zoe</creator><creator>Chui, Helena C</creator><creator>Sullivan, Patrick M</creator><creator>Yassine, Hussein N</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-2483-649X</orcidid></search><sort><creationdate>20220615</creationdate><title>Calcium-dependent cytosolic phospholipase A2 activation is implicated in neuroinflammation and oxidative stress associated with ApoE4</title><author>Wang, Shaowei ; 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The activation of calcium-dependent cytosolic phospholipase A.sub.2 (cPLA2) is involved in inflammatory signaling and is elevated within the plaques of AD brains. The relation between APOE4 genotype and cPLA2 activity is not known. Methods Mouse primary astrocytes, mouse and human brain samples differing by APOE genotypes were collected for measuring cPLA2 expression, phosphorylation, and activity in relation to measures of inflammation and oxidative stress. Results Greater cPLA2 phosphorylation, cPLA2 activity and leukotriene B4 (LTB4) levels were identified in ApoE4 compared to ApoE3 in primary astrocytes, brains of ApoE-targeted replacement (ApoE-TR) mice, and in human brain homogenates from the inferior frontal cortex of persons with AD dementia carrying APOE3/4 compared to APOE3/3. Higher phosphorylated p38 MAPK but not ERK1/2 was found in ApoE4 primary astrocytes and mouse brains than that in ApoE3. Greater cPLA2 translocation to cytosol was observed in human postmortem frontal cortical synaptosomes with recombinant ApoE4 than ApoE3 ex vivo. In ApoE4 astrocytes, the greater levels of LTB4, reactive oxygen species (ROS), and inducible nitric oxide synthase (iNOS) were reduced after cPLA2 inhibition. Conclusions Our findings implicate greater activation of cPLA2 signaling system with APOE4, which could represent a potential drug target for mitigating the increased neuroinflammation with APOE4 and AD. Keywords: cPLA2, ApoE4, Alzheimer's disease, p38 MAPK, Neuroinflammation, Oxidative stress</abstract><cop>London</cop><pub>BioMed Central Ltd</pub><pmid>35705959</pmid><doi>10.1186/s13024-022-00549-5</doi><tpages>21</tpages><orcidid>https://orcid.org/0000-0002-2483-649X</orcidid><oa>free_for_read</oa></addata></record>
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subjects Advertising executives
Alzheimer's disease
Antibodies
ApoE4
Apolipoprotein E
Apolipoprotein E4
Apolipoproteins
Astrocytes
Brain
Calcium
Cortex (frontal)
cPLA2
Cyclin-dependent kinases
Cytosol
Dementia
Dementia disorders
Development and progression
Enzymes
Fatty acids
Genotypes
Inflammation
Kinases
Leukotriene B4
MAP kinase
Metabolism
Neurodegenerative diseases
Neuroinflammation
Nitric oxide
Nitric-oxide synthase
Oxidative stress
p38 MAPK
Phospholipase A2
Phospholipases
Phosphorylation
Plaques
Proteins
Reactive oxygen species
Synaptosomes
Target marketing
Therapeutic targets
title Calcium-dependent cytosolic phospholipase A2 activation is implicated in neuroinflammation and oxidative stress associated with ApoE4
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