Statin action enriches HDL3 in polyunsaturated phospholipids and plasmalogens and reduces LDL-derived phospholipid hydroperoxides in atherogenic mixed dyslipidemia.
Identifieur interne : 001657 ( PubMed/Corpus ); précédent : 001656; suivant : 001658Statin action enriches HDL3 in polyunsaturated phospholipids and plasmalogens and reduces LDL-derived phospholipid hydroperoxides in atherogenic mixed dyslipidemia.
Auteurs : Alexina Orsoni ; Patrice Thérond ; Ricardo Tan ; Philippe Giral ; Paul Robillard ; Anatol Kontush ; Peter J. Meikle ; M John ChapmanSource :
- Journal of lipid research [ 1539-7262 ] ; 2016.
English descriptors
- KwdEn :
- Adult, Aged, Antioxidants (administration & dosage), Apolipoprotein A-I (blood), Cholesterol, HDL (blood), Cholesterol, LDL (blood), Dyslipidemias (blood), Dyslipidemias (drug therapy), Dyslipidemias (pathology), Female, Humans, Male, Middle Aged, Oxidative Stress (drug effects), Quinolines (administration & dosage).
- MESH :
- chemical , administration & dosage : Antioxidants, Quinolines.
- chemical , blood : Apolipoprotein A-I, Cholesterol, HDL, Cholesterol, LDL.
- blood : Dyslipidemias.
- drug effects : Oxidative Stress.
- drug therapy : Dyslipidemias.
- pathology : Dyslipidemias.
- Adult, Aged, Female, Humans, Male, Middle Aged.
Abstract
Atherogenic mixed dyslipidemia associates with oxidative stress and defective HDL antioxidative function in metabolic syndrome (MetS). The impact of statin treatment on the capacity of HDL to inactivate LDL-derived, redox-active phospholipid hydroperoxides (PCOOHs) in MetS is indeterminate. Insulin-resistant, hypertriglyceridemic, hypertensive, obese males were treated with pitavastatin (4 mg/day) for 180 days, resulting in marked reduction in plasma TGs (-41%) and LDL-cholesterol (-38%), with minor effects on HDL-cholesterol and apoAI. Native plasma LDL (baseline vs. 180 days) was oxidized by aqueous free radicals under mild conditions in vitro either alone or in the presence of the corresponding pre- or poststatin HDL2 or HDL3 at authentic plasma mass ratios. Lipidomic analyses revealed that statin treatment i) reduced the content of oxidizable polyunsaturated phosphatidylcholine (PUPC) species containing DHA and linoleic acid in LDL; ii) preferentially increased the content of PUPC species containing arachidonic acid (AA) in small, dense HDL3; iii) induced significant elevation in the content of phosphatidylcholine and phosphatidylethanolamine (PE) plasmalogens containing AA and DHA in HDL3; and iv) induced formation of HDL3 particles with increased capacity to inactivate PCOOH with formation of redox-inactive phospholipid hydroxide. Statin action attenuated LDL oxidability Concomitantly, the capacity of HDL3 to inactivate redox-active PCOOH was enhanced relative to HDL2, consistent with preferential enrichment of PE plasmalogens and PUPC in HDL3.
DOI: 10.1194/jlr.P068585
PubMed: 27581680
Links to Exploration step
pubmed:27581680Le document en format XML
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Meikle</name><affiliation><nlm:affiliation>Baker IDI Heart and Diabetes Institute, Melbourne, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Chapman, M John" sort="Chapman, M John" uniqKey="Chapman M" first="M John" last="Chapman">M John Chapman</name><affiliation><nlm:affiliation>Clinical Biochemistry Service, APHP, HUPS, Bicêtre University Hospital, Le Kremlin Bicêtre, France john.chapman@upmc.fr.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27581680</idno><idno type="pmid">27581680</idno><idno type="doi">10.1194/jlr.P068585</idno><idno type="wicri:Area/PubMed/Corpus">001657</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001657</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Statin action enriches HDL3 in polyunsaturated phospholipids and plasmalogens and reduces LDL-derived phospholipid hydroperoxides in atherogenic mixed dyslipidemia.</title><author><name sortKey="Orsoni, Alexina" sort="Orsoni, Alexina" uniqKey="Orsoni A" first="Alexina" last="Orsoni">Alexina Orsoni</name><affiliation><nlm:affiliation>Clinical Biochemistry Service, APHP, HUPS, Bicêtre University Hospital, Le Kremlin Bicêtre, France.</nlm:affiliation></affiliation></author><author><name sortKey="Therond, Patrice" sort="Therond, Patrice" uniqKey="Therond P" first="Patrice" last="Thérond">Patrice Thérond</name><affiliation><nlm:affiliation>Clinical Biochemistry Service, APHP, HUPS, Bicêtre University Hospital, Le Kremlin Bicêtre, France.</nlm:affiliation></affiliation></author><author><name sortKey="Tan, Ricardo" sort="Tan, Ricardo" uniqKey="Tan R" first="Ricardo" last="Tan">Ricardo Tan</name><affiliation><nlm:affiliation>Baker IDI Heart and Diabetes Institute, Melbourne, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Giral, Philippe" sort="Giral, Philippe" uniqKey="Giral P" first="Philippe" last="Giral">Philippe Giral</name><affiliation><nlm:affiliation>Service of Endocrinology-Metabolism and Cardiovascular Disease Prevention, Pitié-Salpêtrière University Hospital, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Robillard, Paul" sort="Robillard, Paul" uniqKey="Robillard P" first="Paul" last="Robillard">Paul Robillard</name><affiliation><nlm:affiliation>INSERM UMR-S939, Dyslipidemia and Atherosclerosis, and University of Pierre and Marie Curie, Pitié-Salpêtrière University Hospital, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Kontush, Anatol" sort="Kontush, Anatol" uniqKey="Kontush A" first="Anatol" last="Kontush">Anatol Kontush</name><affiliation><nlm:affiliation>INSERM UMR-S1166 and University of Pierre and Marie Curie, Pitié-Salpêtrière University Hospital, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Meikle, Peter J" sort="Meikle, Peter J" uniqKey="Meikle P" first="Peter J" last="Meikle">Peter J. Meikle</name><affiliation><nlm:affiliation>Baker IDI Heart and Diabetes Institute, Melbourne, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Chapman, M John" sort="Chapman, M John" uniqKey="Chapman M" first="M John" last="Chapman">M John Chapman</name><affiliation><nlm:affiliation>Clinical Biochemistry Service, APHP, HUPS, Bicêtre University Hospital, Le Kremlin Bicêtre, France john.chapman@upmc.fr.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Journal of lipid research</title><idno type="eISSN">1539-7262</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Antioxidants (administration & dosage)</term><term>Apolipoprotein A-I (blood)</term><term>Cholesterol, HDL (blood)</term><term>Cholesterol, LDL (blood)</term><term>Dyslipidemias (blood)</term><term>Dyslipidemias (drug therapy)</term><term>Dyslipidemias (pathology)</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Oxidative Stress (drug effects)</term><term>Quinolines (administration & dosage)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antioxidants</term><term>Quinolines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Apolipoprotein A-I</term><term>Cholesterol, HDL</term><term>Cholesterol, LDL</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Dyslipidemias</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Oxidative Stress</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Dyslipidemias</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dyslipidemias</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Atherogenic mixed dyslipidemia associates with oxidative stress and defective HDL antioxidative function in metabolic syndrome (MetS). The impact of statin treatment on the capacity of HDL to inactivate LDL-derived, redox-active phospholipid hydroperoxides (PCOOHs) in MetS is indeterminate. Insulin-resistant, hypertriglyceridemic, hypertensive, obese males were treated with pitavastatin (4 mg/day) for 180 days, resulting in marked reduction in plasma TGs (-41%) and LDL-cholesterol (-38%), with minor effects on HDL-cholesterol and apoAI. Native plasma LDL (baseline vs. 180 days) was oxidized by aqueous free radicals under mild conditions in vitro either alone or in the presence of the corresponding pre- or poststatin HDL2 or HDL3 at authentic plasma mass ratios. Lipidomic analyses revealed that statin treatment i) reduced the content of oxidizable polyunsaturated phosphatidylcholine (PUPC) species containing DHA and linoleic acid in LDL; ii) preferentially increased the content of PUPC species containing arachidonic acid (AA) in small, dense HDL3; iii) induced significant elevation in the content of phosphatidylcholine and phosphatidylethanolamine (PE) plasmalogens containing AA and DHA in HDL3; and iv) induced formation of HDL3 particles with increased capacity to inactivate PCOOH with formation of redox-inactive phospholipid hydroxide. Statin action attenuated LDL oxidability Concomitantly, the capacity of HDL3 to inactivate redox-active PCOOH was enhanced relative to HDL2, consistent with preferential enrichment of PE plasmalogens and PUPC in HDL3.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27581680</PMID><DateCreated><Year>2016</Year><Month>09</Month><Day>01</Day></DateCreated><DateCompleted><Year>2017</Year><Month>08</Month><Day>14</Day></DateCompleted><DateRevised><Year>2017</Year><Month>11</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1539-7262</ISSN><JournalIssue CitedMedium="Internet"><Volume>57</Volume><Issue>11</Issue><PubDate><Year>2016</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Journal of lipid research</Title><ISOAbbreviation>J. Lipid Res.</ISOAbbreviation></Journal><ArticleTitle>Statin action enriches HDL3 in polyunsaturated phospholipids and plasmalogens and reduces LDL-derived phospholipid hydroperoxides in atherogenic mixed dyslipidemia.</ArticleTitle><Pagination><MedlinePgn>2073-2087</MedlinePgn></Pagination><Abstract><AbstractText>Atherogenic mixed dyslipidemia associates with oxidative stress and defective HDL antioxidative function in metabolic syndrome (MetS). The impact of statin treatment on the capacity of HDL to inactivate LDL-derived, redox-active phospholipid hydroperoxides (PCOOHs) in MetS is indeterminate. Insulin-resistant, hypertriglyceridemic, hypertensive, obese males were treated with pitavastatin (4 mg/day) for 180 days, resulting in marked reduction in plasma TGs (-41%) and LDL-cholesterol (-38%), with minor effects on HDL-cholesterol and apoAI. Native plasma LDL (baseline vs. 180 days) was oxidized by aqueous free radicals under mild conditions in vitro either alone or in the presence of the corresponding pre- or poststatin HDL2 or HDL3 at authentic plasma mass ratios. Lipidomic analyses revealed that statin treatment i) reduced the content of oxidizable polyunsaturated phosphatidylcholine (PUPC) species containing DHA and linoleic acid in LDL; ii) preferentially increased the content of PUPC species containing arachidonic acid (AA) in small, dense HDL3; iii) induced significant elevation in the content of phosphatidylcholine and phosphatidylethanolamine (PE) plasmalogens containing AA and DHA in HDL3; and iv) induced formation of HDL3 particles with increased capacity to inactivate PCOOH with formation of redox-inactive phospholipid hydroxide. Statin action attenuated LDL oxidability Concomitantly, the capacity of HDL3 to inactivate redox-active PCOOH was enhanced relative to HDL2, consistent with preferential enrichment of PE plasmalogens and PUPC in HDL3.</AbstractText><CopyrightInformation>Copyright © 2016 by the American Society for Biochemistry and Molecular Biology, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Orsoni</LastName><ForeName>Alexina</ForeName><Initials>A</Initials><Identifier Source="ORCID">http://orcid.org/0000-0003-4250-6280</Identifier><AffiliationInfo><Affiliation>Clinical Biochemistry Service, APHP, HUPS, Bicêtre University Hospital, Le Kremlin Bicêtre, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thérond</LastName><ForeName>Patrice</ForeName><Initials>P</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-7655-2229</Identifier><AffiliationInfo><Affiliation>Clinical Biochemistry Service, APHP, HUPS, Bicêtre University Hospital, Le Kremlin Bicêtre, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Lip(Sys) Department, Atherosclerosis: Cholesterol Homeostasis and Macrophage Trafficking, Paris-Sud University and Paris-Saclay University, Châtenay-Malabry, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tan</LastName><ForeName>Ricardo</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Baker IDI Heart and Diabetes Institute, Melbourne, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Giral</LastName><ForeName>Philippe</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Service of Endocrinology-Metabolism and Cardiovascular Disease Prevention, Pitié-Salpêtrière University Hospital, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Robillard</LastName><ForeName>Paul</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>INSERM UMR-S939, Dyslipidemia and Atherosclerosis, and University of Pierre and Marie Curie, Pitié-Salpêtrière University Hospital, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kontush</LastName><ForeName>Anatol</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>INSERM UMR-S1166 and University of Pierre and Marie Curie, Pitié-Salpêtrière University Hospital, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meikle</LastName><ForeName>Peter J</ForeName><Initials>PJ</Initials><Identifier Source="ORCID">http://orcid/org/0000-0002-2593-4665</Identifier><AffiliationInfo><Affiliation>Baker IDI Heart and Diabetes Institute, Melbourne, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chapman</LastName><ForeName>M John</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>Clinical Biochemistry Service, APHP, HUPS, Bicêtre University Hospital, Le Kremlin Bicêtre, France john.chapman@upmc.fr.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Service of Endocrinology-Metabolism and Cardiovascular Disease Prevention, Pitié-Salpêtrière University Hospital, Paris, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>INSERM UMR-S939, Dyslipidemia and Atherosclerosis, and University of Pierre and Marie Curie, Pitié-Salpêtrière University Hospital, Paris, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016430">Clinical Trial</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>08</Month><Day>31</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Lipid Res</MedlineTA><NlmUniqueID>0376606</NlmUniqueID><ISSNLinking>0022-2275</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C505693">APOA1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000975">Antioxidants</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016632">Apolipoprotein A-I</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008076">Cholesterol, HDL</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008078">Cholesterol, LDL</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011804">Quinolines</NameOfSubstance></Chemical><Chemical><RegistryNumber>M5681Q5F9P</RegistryNumber><NameOfSubstance 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