Statin action enriches HDL3 in polyunsaturated phospholipids and plasmalogens and reduces LDL-derived phospholipid hydroperoxides in atherogenic mixed dyslipidemia
Identifieur interne : 000598 ( Pmc/Checkpoint ); précédent : 000597; suivant : 000599Statin 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 [ 0022-2275 ] ; 2016.
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
Url:
DOI: 10.1194/jlr.P068585
PubMed: 27581680
PubMed Central: 5087874
Affiliations:
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<author><name sortKey="Therond, Patrice" sort="Therond, Patrice" uniqKey="Therond P" first="Patrice" last="Thérond">Patrice Thérond</name>
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<author><name sortKey="Kontush, Anatol" sort="Kontush, Anatol" uniqKey="Kontush A" first="Anatol" last="Kontush">Anatol Kontush</name>
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<author><name sortKey="Meikle, Peter J" sort="Meikle, Peter J" uniqKey="Meikle P" first="Peter J." last="Meikle">Peter J. Meikle</name>
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<author><name sortKey="Chapman, M John" sort="Chapman, M John" uniqKey="Chapman M" first="M. John" last="Chapman">M. John Chapman</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">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>
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<author><name sortKey="Therond, Patrice" sort="Therond, Patrice" uniqKey="Therond P" first="Patrice" last="Thérond">Patrice Thérond</name>
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<author><name sortKey="Tan, Ricardo" sort="Tan, Ricardo" uniqKey="Tan R" first="Ricardo" last="Tan">Ricardo Tan</name>
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<author><name sortKey="Giral, Philippe" sort="Giral, Philippe" uniqKey="Giral P" first="Philippe" last="Giral">Philippe Giral</name>
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<author><name sortKey="Robillard, Paul" sort="Robillard, Paul" uniqKey="Robillard P" first="Paul" last="Robillard">Paul Robillard</name>
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<author><name sortKey="Kontush, Anatol" sort="Kontush, Anatol" uniqKey="Kontush A" first="Anatol" last="Kontush">Anatol Kontush</name>
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<author><name sortKey="Meikle, Peter J" sort="Meikle, Peter J" uniqKey="Meikle P" first="Peter J." last="Meikle">Peter J. Meikle</name>
<affiliation><nlm:aff id="aff3"></nlm:aff>
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<author><name sortKey="Chapman, M John" sort="Chapman, M John" uniqKey="Chapman M" first="M. John" last="Chapman">M. John Chapman</name>
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<series><title level="j">Journal of Lipid Research</title>
<idno type="ISSN">0022-2275</idno>
<idno type="eISSN">1539-7262</idno>
<imprint><date when="2016">2016</date>
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<front><div type="abstract" xml:lang="en"><p>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
<italic>i</italic>
) reduced the content of oxidizable polyunsaturated
phosphatidylcholine (PUPC) species containing DHA and linoleic acid in LDL;
<italic>ii</italic>
) preferentially increased the content of PUPC species
containing arachidonic acid (AA) in small, dense HDL3; <italic>iii</italic>
)
induced significant elevation in the content of phosphatidylcholine and
phosphatidylethanolamine (PE) plasmalogens containing AA and DHA in HDL3; and
<italic>iv</italic>
) 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.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Lipid Res</journal-id>
<journal-id journal-id-type="iso-abbrev">J. Lipid Res</journal-id>
<journal-id journal-id-type="hwp">jlr</journal-id>
<journal-id journal-id-type="pmc">jlr</journal-id>
<journal-id journal-id-type="publisher-id">jlr</journal-id>
<journal-title-group><journal-title>Journal of Lipid Research</journal-title>
</journal-title-group>
<issn pub-type="ppub">0022-2275</issn>
<issn pub-type="epub">1539-7262</issn>
<publisher><publisher-name>The American Society for Biochemistry and Molecular
Biology</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">27581680</article-id>
<article-id pub-id-type="pmc">5087874</article-id>
<article-id pub-id-type="publisher-id">p068585</article-id>
<article-id pub-id-type="doi">10.1194/jlr.P068585</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Patient-Oriented and Epidemiological Research</subject>
</subj-group>
</article-categories>
<title-group><article-title>Statin action enriches HDL3 in polyunsaturated phospholipids and
plasmalogens and reduces LDL-derived phospholipid hydroperoxides in atherogenic
mixed dyslipidemia</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0003-4250-6280</contrib-id>
<name><surname>Orsoni</surname>
<given-names>Alexina</given-names>
</name>
<xref ref-type="aff" rid="aff1">*</xref>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0002-7655-2229</contrib-id>
<name><surname>Thérond</surname>
<given-names>Patrice</given-names>
</name>
<xref ref-type="aff" rid="aff1">*</xref>
<xref ref-type="aff" rid="aff2">†</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Tan</surname>
<given-names>Ricardo</given-names>
</name>
<xref ref-type="aff" rid="aff3">§</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Giral</surname>
<given-names>Philippe</given-names>
</name>
<xref ref-type="aff" rid="aff4">**</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Robillard</surname>
<given-names>Paul</given-names>
</name>
<xref ref-type="aff" rid="aff5">††</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kontush</surname>
<given-names>Anatol</given-names>
</name>
<xref ref-type="aff" rid="aff6">§§</xref>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0002-2593-4665</contrib-id>
<name><surname>Meikle</surname>
<given-names>Peter J.</given-names>
</name>
<xref ref-type="aff" rid="aff3">§</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chapman</surname>
<given-names>M. John</given-names>
</name>
<xref ref-type="corresp" rid="cor1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff1">*</xref>
<xref ref-type="aff" rid="aff4">**</xref>
<xref ref-type="aff" rid="aff5">††</xref>
</contrib>
<aff id="aff1">Clinical Biochemistry Service,<label>*</label>
<institution>APHP, HUPS, Bicêtre University Hospital</institution>
, Le Kremlin Bicêtre,<country>France</country>
</aff>
<aff id="aff2">Lip(Sys)<sup>2</sup>
Department, Atherosclerosis: Cholesterol Homeostasis and Macrophage Trafficking,<label>†</label>
<institution>Paris-Sud University and Paris-Saclay University</institution>
, Châtenay-Malabry,<country>France</country>
</aff>
<aff id="aff3"><institution>Baker IDI Heart and Diabetes Institute</institution>
,<label>§</label>
Melbourne,<country>Australia</country>
</aff>
<aff id="aff4">Service of Endocrinology-Metabolism and Cardiovascular Disease Prevention,<label>**</label>
<institution>Pitié-Salpêtrière University Hospital</institution>
, Paris,<country>France</country>
</aff>
<aff id="aff5">INSERM UMR-S939, Dyslipidemia and Atherosclerosis, and University of Pierre and Marie Curie,<label>††</label>
<institution>Pitié-Salpêtrière University Hospital</institution>
, Paris,<country>France</country>
</aff>
<aff id="aff6">INSERM UMR-S1166 and University of Pierre and Marie Curie,<label>§§</label>
<institution>Pitié-Salpêtrière University Hospital</institution>
, Paris,<country>France</country>
</aff>
</contrib-group>
<author-notes><corresp id="cor1"><label>1</label>
To whom correspondence should be addressed.
e-mail: <email>john.chapman@upmc.fr</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>11</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="epub"><day>27</day>
<month>10</month>
<year>2016</year>
</pub-date>
<volume>57</volume>
<issue>11</issue>
<fpage>2073</fpage>
<lpage>2087</lpage>
<history><date date-type="received"><day>19</day>
<month>4</month>
<year>2016</year>
</date>
<date date-type="rev-recd"><day>16</day>
<month>8</month>
<year>2016</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2016 by the American Society for
Biochemistry and Molecular Biology, Inc.</copyright-statement>
<copyright-year>2016</copyright-year>
</permissions>
<abstract><p>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
<italic>i</italic>
) reduced the content of oxidizable polyunsaturated
phosphatidylcholine (PUPC) species containing DHA and linoleic acid in LDL;
<italic>ii</italic>
) preferentially increased the content of PUPC species
containing arachidonic acid (AA) in small, dense HDL3; <italic>iii</italic>
)
induced significant elevation in the content of phosphatidylcholine and
phosphatidylethanolamine (PE) plasmalogens containing AA and DHA in HDL3; and
<italic>iv</italic>
) 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.</p>
</abstract>
<kwd-group><kwd>antioxidative activity</kwd>
<kwd>low density lipoprotein</kwd>
<kwd>high density lipoprotein 3</kwd>
<kwd>lipidomics</kwd>
<kwd>metabolic syndrome disease</kwd>
<kwd>pitavastatin</kwd>
<kwd>oxidative stress</kwd>
<kwd>phospholipid hydroxides</kwd>
</kwd-group>
<funding-group><award-group id="sp1"><funding-source>Institut National de la Santé et de la Recherche
Médicale<named-content content-type="funder-id">http://dx.doi.org/10.13039/501100001677</named-content>
</funding-source>
</award-group>
</funding-group>
<funding-group><award-group id="sp2"><funding-source>National Health and Medical Research Council<named-content content-type="funder-id">http://dx.doi.org/10.13039/501100000925</named-content>
</funding-source>
</award-group>
</funding-group>
<funding-group><award-group id="sp3"><funding-source>State Government of Victoria<named-content content-type="funder-id">http://dx.doi.org/10.13039/501100004752</named-content>
</funding-source>
</award-group>
</funding-group>
</article-meta>
</front>
</pmc>
<affiliations><list></list>
<tree><noCountry><name sortKey="Chapman, M John" sort="Chapman, M John" uniqKey="Chapman M" first="M. John" last="Chapman">M. John Chapman</name>
<name sortKey="Giral, Philippe" sort="Giral, Philippe" uniqKey="Giral P" first="Philippe" last="Giral">Philippe Giral</name>
<name sortKey="Kontush, Anatol" sort="Kontush, Anatol" uniqKey="Kontush A" first="Anatol" last="Kontush">Anatol Kontush</name>
<name sortKey="Meikle, Peter J" sort="Meikle, Peter J" uniqKey="Meikle P" first="Peter J." last="Meikle">Peter J. Meikle</name>
<name sortKey="Orsoni, Alexina" sort="Orsoni, Alexina" uniqKey="Orsoni A" first="Alexina" last="Orsoni">Alexina Orsoni</name>
<name sortKey="Robillard, Paul" sort="Robillard, Paul" uniqKey="Robillard P" first="Paul" last="Robillard">Paul Robillard</name>
<name sortKey="Tan, Ricardo" sort="Tan, Ricardo" uniqKey="Tan R" first="Ricardo" last="Tan">Ricardo Tan</name>
<name sortKey="Therond, Patrice" sort="Therond, Patrice" uniqKey="Therond P" first="Patrice" last="Thérond">Patrice Thérond</name>
</noCountry>
</tree>
</affiliations>
</record>
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