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The apolipoprotein A-I mimetic peptide, D-4F, restrains neointimal formation through heme oxygenase-1 up-regulation.

Identifieur interne : 000B27 ( Main/Exploration ); précédent : 000B26; suivant : 000B28

The apolipoprotein A-I mimetic peptide, D-4F, restrains neointimal formation through heme oxygenase-1 up-regulation.

Auteurs : Donghui Liu [République populaire de Chine] ; Mengzhang Wu [République populaire de Chine] ; Qian Du [République populaire de Chine] ; Zhenzhen Ding [République populaire de Chine] ; Mingming Qian [République populaire de Chine] ; Zijia Tong [République populaire de Chine] ; Wenqi Xu [République populaire de Chine] ; Le Zhang [République populaire de Chine] ; He Chang [République populaire de Chine] ; Yan Wang [République populaire de Chine] ; Caihua Huang [République populaire de Chine] ; Donghai Lin [République populaire de Chine]

Source :

RBID : pubmed:28767201

Descripteurs français

English descriptors

Abstract

D-4F, an apolipoprotein A-I (apoA-I) mimetic peptide, possesses distinctly anti-atherogenic effects. However, the biological functions and mechanisms of D-4F on the hyperplasia of vascular smooth muscle cells (VSMCs) remain unclear. This study aimed to determine its roles in the proliferation and migration of VSMCs. In vitro, D-4F inhibited VSMC proliferation and migration induced by ox-LDL in a dose-dependent manner. D-4F up-regulated heme oxygenase-1 (HO-1) expression in VSMCs, and the PI3K/Akt/AMP-activated protein kinase (AMPK) pathway was involved in these processes. HO-1 down-regulation with siRNA or inhibition with zinc protoporphyrin (Znpp) impaired the protective effects of D-4F on the oxidative stress and the proliferation and migration of VSMCs. Moreover, down-regulation of ATP-binding cassette transporter A1 (ABCA1) abolished the activation of Akt and AMPK, the up-regulation of HO-1 and the anti-oxidative effects of D-4F. In vivo, D-4F restrained neointimal formation and oxidative stress of carotid arteries in balloon-injured Sprague Dawley rats. And inhibition of HO-1 with Znpp decreased the inhibitory effects of D-4F on neointimal formation and ROS production in arteries. In conclusion, D-4F inhibited VSMC proliferation and migration in vitro and neointimal formation in vivo through HO-1 up-regulation, which provided a novel prophylactic and therapeutic strategy for anti-restenosis of arteries.

DOI: 10.1111/jcmm.13290
PubMed: 28767201
PubMed Central: PMC5706511


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<name sortKey="Lin, Donghai" sort="Lin, Donghai" uniqKey="Lin D" first="Donghai" last="Lin">Donghai Lin</name>
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<wicri:noRegion>Xiamen</wicri:noRegion>
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<nlm:affiliation>Union Clinical Medical College of Fujian Medical University, Fuzhou, China.</nlm:affiliation>
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<wicri:regionArea>Union Clinical Medical College of Fujian Medical University, Fuzhou</wicri:regionArea>
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<name sortKey="Qian, Mingming" sort="Qian, Mingming" uniqKey="Qian M" first="Mingming" last="Qian">Mingming Qian</name>
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<nlm:affiliation>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen</wicri:regionArea>
<wicri:noRegion>Xiamen</wicri:noRegion>
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<name sortKey="Tong, Zijia" sort="Tong, Zijia" uniqKey="Tong Z" first="Zijia" last="Tong">Zijia Tong</name>
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<nlm:affiliation>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen</wicri:regionArea>
<wicri:noRegion>Xiamen</wicri:noRegion>
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<nlm:affiliation>Union Clinical Medical College of Fujian Medical University, Fuzhou, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Union Clinical Medical College of Fujian Medical University, Fuzhou</wicri:regionArea>
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<settlement type="city">Fuzhou</settlement>
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<name sortKey="Xu, Wenqi" sort="Xu, Wenqi" uniqKey="Xu W" first="Wenqi" last="Xu">Wenqi Xu</name>
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<nlm:affiliation>High-field NMR Research Center, MOE Key Laboratory of Spectrochemical Analysis & Instrumentation, College of Chemistry and Chemical Engineering, Xiamen University, Xiamen, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>High-field NMR Research Center, MOE Key Laboratory of Spectrochemical Analysis & Instrumentation, College of Chemistry and Chemical Engineering, Xiamen University, Xiamen</wicri:regionArea>
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<name sortKey="Zhang, Le" sort="Zhang, Le" uniqKey="Zhang L" first="Le" last="Zhang">Le Zhang</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen</wicri:regionArea>
<wicri:noRegion>Xiamen</wicri:noRegion>
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<name sortKey="Chang, He" sort="Chang, He" uniqKey="Chang H" first="He" last="Chang">He Chang</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen</wicri:regionArea>
<wicri:noRegion>Xiamen</wicri:noRegion>
</affiliation>
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<author>
<name sortKey="Wang, Yan" sort="Wang, Yan" uniqKey="Wang Y" first="Yan" last="Wang">Yan Wang</name>
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<nlm:affiliation>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen</wicri:regionArea>
<wicri:noRegion>Xiamen</wicri:noRegion>
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<name sortKey="Huang, Caihua" sort="Huang, Caihua" uniqKey="Huang C" first="Caihua" last="Huang">Caihua Huang</name>
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<nlm:affiliation>Department of Physical Education, Xiamen University of Technology, Xiamen, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Physical Education, Xiamen University of Technology, Xiamen</wicri:regionArea>
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<name sortKey="Lin, Donghai" sort="Lin, Donghai" uniqKey="Lin D" first="Donghai" last="Lin">Donghai Lin</name>
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<title level="j">Journal of cellular and molecular medicine</title>
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<term>AMP-Activated Protein Kinases (genetics)</term>
<term>AMP-Activated Protein Kinases (metabolism)</term>
<term>ATP Binding Cassette Transporter 1 (genetics)</term>
<term>ATP Binding Cassette Transporter 1 (metabolism)</term>
<term>Animals (MeSH)</term>
<term>Aorta, Thoracic (cytology)</term>
<term>Aorta, Thoracic (drug effects)</term>
<term>Aorta, Thoracic (metabolism)</term>
<term>Apolipoprotein A-I (pharmacology)</term>
<term>Atherosclerosis (genetics)</term>
<term>Atherosclerosis (metabolism)</term>
<term>Atherosclerosis (pathology)</term>
<term>Atherosclerosis (prevention & control)</term>
<term>Cell Movement (drug effects)</term>
<term>Cell Proliferation (drug effects)</term>
<term>Gene Expression Regulation (MeSH)</term>
<term>Heme Oxygenase-1 (genetics)</term>
<term>Heme Oxygenase-1 (metabolism)</term>
<term>Lipoproteins, LDL (antagonists & inhibitors)</term>
<term>Lipoproteins, LDL (pharmacology)</term>
<term>Male (MeSH)</term>
<term>Muscle, Smooth, Vascular (cytology)</term>
<term>Muscle, Smooth, Vascular (drug effects)</term>
<term>Muscle, Smooth, Vascular (metabolism)</term>
<term>Myocytes, Smooth Muscle (cytology)</term>
<term>Myocytes, Smooth Muscle (drug effects)</term>
<term>Myocytes, Smooth Muscle (metabolism)</term>
<term>Neointima (genetics)</term>
<term>Neointima (metabolism)</term>
<term>Neointima (pathology)</term>
<term>Neointima (prevention & control)</term>
<term>Phosphatidylinositol 3-Kinases (genetics)</term>
<term>Phosphatidylinositol 3-Kinases (metabolism)</term>
<term>Protective Agents (pharmacology)</term>
<term>Proto-Oncogene Proteins c-akt (genetics)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>Rats (MeSH)</term>
<term>Rats, Sprague-Dawley (MeSH)</term>
<term>Signal Transduction (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr">
<term>AMP-Activated Protein Kinases (génétique)</term>
<term>AMP-Activated Protein Kinases (métabolisme)</term>
<term>Agents protecteurs (pharmacologie)</term>
<term>Animaux (MeSH)</term>
<term>Aorte thoracique (cytologie)</term>
<term>Aorte thoracique (effets des médicaments et des substances chimiques)</term>
<term>Aorte thoracique (métabolisme)</term>
<term>Apolipoprotéine A-I (pharmacologie)</term>
<term>Athérosclérose (anatomopathologie)</term>
<term>Athérosclérose (génétique)</term>
<term>Athérosclérose (métabolisme)</term>
<term>Athérosclérose (prévention et contrôle)</term>
<term>Heme oxygenase-1 (génétique)</term>
<term>Heme oxygenase-1 (métabolisme)</term>
<term>Lipoprotéines LDL (antagonistes et inhibiteurs)</term>
<term>Lipoprotéines LDL (pharmacologie)</term>
<term>Membre-1 de la sous-famille A des transporteurs à cassette liant l'ATP (génétique)</term>
<term>Membre-1 de la sous-famille A des transporteurs à cassette liant l'ATP (métabolisme)</term>
<term>Mouvement cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Muscles lisses vasculaires (cytologie)</term>
<term>Muscles lisses vasculaires (effets des médicaments et des substances chimiques)</term>
<term>Muscles lisses vasculaires (métabolisme)</term>
<term>Myocytes du muscle lisse (cytologie)</term>
<term>Myocytes du muscle lisse (effets des médicaments et des substances chimiques)</term>
<term>Myocytes du muscle lisse (métabolisme)</term>
<term>Mâle (MeSH)</term>
<term>Néointima (anatomopathologie)</term>
<term>Néointima (génétique)</term>
<term>Néointima (métabolisme)</term>
<term>Néointima (prévention et contrôle)</term>
<term>Phosphatidylinositol 3-kinases (génétique)</term>
<term>Phosphatidylinositol 3-kinases (métabolisme)</term>
<term>Prolifération cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Protéines proto-oncogènes c-akt (génétique)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Rat Sprague-Dawley (MeSH)</term>
<term>Rats (MeSH)</term>
<term>Régulation de l'expression des gènes (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en">
<term>Lipoproteins, LDL</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en">
<term>AMP-Activated Protein Kinases</term>
<term>ATP Binding Cassette Transporter 1</term>
<term>Heme Oxygenase-1</term>
<term>Phosphatidylinositol 3-Kinases</term>
<term>Proto-Oncogene Proteins c-akt</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en">
<term>AMP-Activated Protein Kinases</term>
<term>ATP Binding Cassette Transporter 1</term>
<term>Heme Oxygenase-1</term>
<term>Phosphatidylinositol 3-Kinases</term>
<term>Proto-Oncogene Proteins c-akt</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr">
<term>Athérosclérose</term>
<term>Néointima</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr">
<term>Lipoprotéines LDL</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr">
<term>Aorte thoracique</term>
<term>Muscles lisses vasculaires</term>
<term>Myocytes du muscle lisse</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en">
<term>Aorta, Thoracic</term>
<term>Muscle, Smooth, Vascular</term>
<term>Myocytes, Smooth Muscle</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en">
<term>Aorta, Thoracic</term>
<term>Cell Movement</term>
<term>Cell Proliferation</term>
<term>Muscle, Smooth, Vascular</term>
<term>Myocytes, Smooth Muscle</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr">
<term>Aorte thoracique</term>
<term>Mouvement cellulaire</term>
<term>Muscles lisses vasculaires</term>
<term>Myocytes du muscle lisse</term>
<term>Prolifération cellulaire</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en">
<term>Atherosclerosis</term>
<term>Neointima</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr">
<term>AMP-Activated Protein Kinases</term>
<term>Athérosclérose</term>
<term>Heme oxygenase-1</term>
<term>Membre-1 de la sous-famille A des transporteurs à cassette liant l'ATP</term>
<term>Néointima</term>
<term>Phosphatidylinositol 3-kinases</term>
<term>Protéines proto-oncogènes c-akt</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en">
<term>Aorta, Thoracic</term>
<term>Atherosclerosis</term>
<term>Muscle, Smooth, Vascular</term>
<term>Myocytes, Smooth Muscle</term>
<term>Neointima</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr">
<term>AMP-Activated Protein Kinases</term>
<term>Aorte thoracique</term>
<term>Athérosclérose</term>
<term>Heme oxygenase-1</term>
<term>Membre-1 de la sous-famille A des transporteurs à cassette liant l'ATP</term>
<term>Muscles lisses vasculaires</term>
<term>Myocytes du muscle lisse</term>
<term>Néointima</term>
<term>Phosphatidylinositol 3-kinases</term>
<term>Protéines proto-oncogènes c-akt</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en">
<term>Atherosclerosis</term>
<term>Neointima</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr">
<term>Agents protecteurs</term>
<term>Apolipoprotéine A-I</term>
<term>Lipoprotéines LDL</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en">
<term>Apolipoprotein A-I</term>
<term>Lipoproteins, LDL</term>
<term>Protective Agents</term>
</keywords>
<keywords scheme="MESH" qualifier="prevention & control" xml:lang="en">
<term>Atherosclerosis</term>
<term>Neointima</term>
</keywords>
<keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr">
<term>Athérosclérose</term>
<term>Néointima</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Animals</term>
<term>Gene Expression Regulation</term>
<term>Male</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr">
<term>Animaux</term>
<term>Mâle</term>
<term>Rat Sprague-Dawley</term>
<term>Rats</term>
<term>Régulation de l'expression des gènes</term>
<term>Transduction du signal</term>
</keywords>
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</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">D-4F, an apolipoprotein A-I (apoA-I) mimetic peptide, possesses distinctly anti-atherogenic effects. However, the biological functions and mechanisms of D-4F on the hyperplasia of vascular smooth muscle cells (VSMCs) remain unclear. This study aimed to determine its roles in the proliferation and migration of VSMCs. In vitro, D-4F inhibited VSMC proliferation and migration induced by ox-LDL in a dose-dependent manner. D-4F up-regulated heme oxygenase-1 (HO-1) expression in VSMCs, and the PI3K/Akt/AMP-activated protein kinase (AMPK) pathway was involved in these processes. HO-1 down-regulation with siRNA or inhibition with zinc protoporphyrin (Znpp) impaired the protective effects of D-4F on the oxidative stress and the proliferation and migration of VSMCs. Moreover, down-regulation of ATP-binding cassette transporter A1 (ABCA1) abolished the activation of Akt and AMPK, the up-regulation of HO-1 and the anti-oxidative effects of D-4F. In vivo, D-4F restrained neointimal formation and oxidative stress of carotid arteries in balloon-injured Sprague Dawley rats. And inhibition of HO-1 with Znpp decreased the inhibitory effects of D-4F on neointimal formation and ROS production in arteries. In conclusion, D-4F inhibited VSMC proliferation and migration in vitro and neointimal formation in vivo through HO-1 up-regulation, which provided a novel prophylactic and therapeutic strategy for anti-restenosis of arteries.</div>
</front>
</TEI>
<pubmed>
<MedlineCitation Status="MEDLINE" Owner="NLM">
<PMID Version="1">28767201</PMID>
<DateCompleted>
<Year>2018</Year>
<Month>07</Month>
<Day>18</Day>
</DateCompleted>
<DateRevised>
<Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic">
<Journal>
<ISSN IssnType="Electronic">1582-4934</ISSN>
<JournalIssue CitedMedium="Internet">
<Volume>21</Volume>
<Issue>12</Issue>
<PubDate>
<Year>2017</Year>
<Month>Dec</Month>
</PubDate>
</JournalIssue>
<Title>Journal of cellular and molecular medicine</Title>
<ISOAbbreviation>J Cell Mol Med</ISOAbbreviation>
</Journal>
<ArticleTitle>The apolipoprotein A-I mimetic peptide, D-4F, restrains neointimal formation through heme oxygenase-1 up-regulation.</ArticleTitle>
<Pagination>
<MedlinePgn>3810-3820</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1111/jcmm.13290</ELocationID>
<Abstract>
<AbstractText>D-4F, an apolipoprotein A-I (apoA-I) mimetic peptide, possesses distinctly anti-atherogenic effects. However, the biological functions and mechanisms of D-4F on the hyperplasia of vascular smooth muscle cells (VSMCs) remain unclear. This study aimed to determine its roles in the proliferation and migration of VSMCs. In vitro, D-4F inhibited VSMC proliferation and migration induced by ox-LDL in a dose-dependent manner. D-4F up-regulated heme oxygenase-1 (HO-1) expression in VSMCs, and the PI3K/Akt/AMP-activated protein kinase (AMPK) pathway was involved in these processes. HO-1 down-regulation with siRNA or inhibition with zinc protoporphyrin (Znpp) impaired the protective effects of D-4F on the oxidative stress and the proliferation and migration of VSMCs. Moreover, down-regulation of ATP-binding cassette transporter A1 (ABCA1) abolished the activation of Akt and AMPK, the up-regulation of HO-1 and the anti-oxidative effects of D-4F. In vivo, D-4F restrained neointimal formation and oxidative stress of carotid arteries in balloon-injured Sprague Dawley rats. And inhibition of HO-1 with Znpp decreased the inhibitory effects of D-4F on neointimal formation and ROS production in arteries. In conclusion, D-4F inhibited VSMC proliferation and migration in vitro and neointimal formation in vivo through HO-1 up-regulation, which provided a novel prophylactic and therapeutic strategy for anti-restenosis of arteries.</AbstractText>
<CopyrightInformation>© 2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y">
<Author ValidYN="Y">
<LastName>Liu</LastName>
<ForeName>Donghui</ForeName>
<Initials>D</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0001-6568-5424</Identifier>
<AffiliationInfo>
<Affiliation>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Wu</LastName>
<ForeName>Mengzhang</ForeName>
<Initials>M</Initials>
<AffiliationInfo>
<Affiliation>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Union Clinical Medical College of Fujian Medical University, Fuzhou, China.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Du</LastName>
<ForeName>Qian</ForeName>
<Initials>Q</Initials>
<AffiliationInfo>
<Affiliation>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Ding</LastName>
<ForeName>Zhenzhen</ForeName>
<Initials>Z</Initials>
<AffiliationInfo>
<Affiliation>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Union Clinical Medical College of Fujian Medical University, Fuzhou, China.</Affiliation>
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<LastName>Qian</LastName>
<ForeName>Mingming</ForeName>
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<Affiliation>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Tong</LastName>
<ForeName>Zijia</ForeName>
<Initials>Z</Initials>
<AffiliationInfo>
<Affiliation>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Union Clinical Medical College of Fujian Medical University, Fuzhou, China.</Affiliation>
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</Author>
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<LastName>Xu</LastName>
<ForeName>Wenqi</ForeName>
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<AffiliationInfo>
<Affiliation>High-field NMR Research Center, MOE Key Laboratory of Spectrochemical Analysis & Instrumentation, College of Chemistry and Chemical Engineering, Xiamen University, Xiamen, China.</Affiliation>
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</Author>
<Author ValidYN="Y">
<LastName>Zhang</LastName>
<ForeName>Le</ForeName>
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<AffiliationInfo>
<Affiliation>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Chang</LastName>
<ForeName>He</ForeName>
<Initials>H</Initials>
<AffiliationInfo>
<Affiliation>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Wang</LastName>
<ForeName>Yan</ForeName>
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<AffiliationInfo>
<Affiliation>Department of Cardiology, The Affiliated Cardiovascular Hospital of Xiamen University, Medical College of Xiamen University, Xiamen, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Huang</LastName>
<ForeName>Caihua</ForeName>
<Initials>C</Initials>
<AffiliationInfo>
<Affiliation>Department of Physical Education, Xiamen University of Technology, Xiamen, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Lin</LastName>
<ForeName>Donghai</ForeName>
<Initials>D</Initials>
<AffiliationInfo>
<Affiliation>High-field NMR Research Center, MOE Key Laboratory of Spectrochemical Analysis & Instrumentation, College of Chemistry and Chemical Engineering, Xiamen University, Xiamen, China.</Affiliation>
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<Year>2017</Year>
<Month>08</Month>
<Day>02</Day>
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<Country>England</Country>
<MedlineTA>J Cell Mol Med</MedlineTA>
<NlmUniqueID>101083777</NlmUniqueID>
<ISSNLinking>1582-1838</ISSNLinking>
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<Chemical>
<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C577834">ABCA1 protein, rat</NameOfSubstance>
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<Chemical>
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<Chemical>
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<Chemical>
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</Chemical>
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<Chemical>
<RegistryNumber>EC 1.14.14.18</RegistryNumber>
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<RegistryNumber>EC 2.7.1.-</RegistryNumber>
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<Chemical>
<RegistryNumber>EC 2.7.11.1</RegistryNumber>
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<RefSource>Front Pharmacol. 2017 Sep 29;8:708</RefSource>
<PMID Version="1">29033843</PMID>
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<MeshHeading>
<DescriptorName UI="D055372" MajorTopicYN="N">AMP-Activated Protein Kinases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D064286" MajorTopicYN="N">ATP Binding Cassette Transporter 1</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading>
<DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
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<MeshHeading>
<DescriptorName UI="D001013" MajorTopicYN="N">Aorta, Thoracic</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D016632" MajorTopicYN="N">Apolipoprotein A-I</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D050197" MajorTopicYN="N">Atherosclerosis</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D002465" MajorTopicYN="N">Cell Movement</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName>
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<MeshHeading>
<DescriptorName UI="D051547" MajorTopicYN="N">Heme Oxygenase-1</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D008077" MajorTopicYN="N">Lipoproteins, LDL</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
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<MeshHeading>
<DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
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<MeshHeading>
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<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
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<MeshHeading>
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<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D058426" MajorTopicYN="N">Neointima</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName>
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<MeshHeading>
<DescriptorName UI="D019869" MajorTopicYN="N">Phosphatidylinositol 3-Kinases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading>
<DescriptorName UI="D020011" MajorTopicYN="N">Protective Agents</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
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<MeshHeading>
<DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading>
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<MeshHeading>
<DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName>
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<MeshHeading>
<DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
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<Keyword MajorTopicYN="N">HO-1</Keyword>
<Keyword MajorTopicYN="N">apoA-I mimetic peptide</Keyword>
<Keyword MajorTopicYN="N">migration</Keyword>
<Keyword MajorTopicYN="N">proliferation</Keyword>
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