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 : 000B28The 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 :
- Journal of cellular and molecular medicine [ 1582-4934 ] ; 2017.
Descripteurs français
- KwdFr :
- AMP-Activated Protein Kinases (génétique), AMP-Activated Protein Kinases (métabolisme), Agents protecteurs (pharmacologie), Animaux (MeSH), Aorte thoracique (cytologie), Aorte thoracique (effets des médicaments et des substances chimiques), Aorte thoracique (métabolisme), Apolipoprotéine A-I (pharmacologie), Athérosclérose (anatomopathologie), Athérosclérose (génétique), Athérosclérose (métabolisme), Athérosclérose (prévention et contrôle), Heme oxygenase-1 (génétique), Heme oxygenase-1 (métabolisme), Lipoprotéines LDL (antagonistes et inhibiteurs), Lipoprotéines LDL (pharmacologie), Membre-1 de la sous-famille A des transporteurs à cassette liant l'ATP (génétique), Membre-1 de la sous-famille A des transporteurs à cassette liant l'ATP (métabolisme), Mouvement cellulaire (effets des médicaments et des substances chimiques), Muscles lisses vasculaires (cytologie), Muscles lisses vasculaires (effets des médicaments et des substances chimiques), Muscles lisses vasculaires (métabolisme), Myocytes du muscle lisse (cytologie), Myocytes du muscle lisse (effets des médicaments et des substances chimiques), Myocytes du muscle lisse (métabolisme), Mâle (MeSH), Néointima (anatomopathologie), Néointima (génétique), Néointima (métabolisme), Néointima (prévention et contrôle), Phosphatidylinositol 3-kinases (génétique), Phosphatidylinositol 3-kinases (métabolisme), Prolifération cellulaire (effets des médicaments et des substances chimiques), Protéines proto-oncogènes c-akt (génétique), Protéines proto-oncogènes c-akt (métabolisme), Rat Sprague-Dawley (MeSH), Rats (MeSH), Régulation de l'expression des gènes (MeSH), Transduction du signal (MeSH).
- MESH :
- anatomopathologie : Athérosclérose, Néointima.
- antagonistes et inhibiteurs : Lipoprotéines LDL.
- cytologie : Aorte thoracique, Muscles lisses vasculaires, Myocytes du muscle lisse.
- effets des médicaments et des substances chimiques : Aorte thoracique, Mouvement cellulaire, Muscles lisses vasculaires, Myocytes du muscle lisse, Prolifération cellulaire.
- génétique : AMP-Activated Protein Kinases, Athérosclérose, Heme oxygenase-1, Membre-1 de la sous-famille A des transporteurs à cassette liant l'ATP, Néointima, Phosphatidylinositol 3-kinases, Protéines proto-oncogènes c-akt.
- métabolisme : AMP-Activated Protein Kinases, Aorte thoracique, Athérosclérose, Heme oxygenase-1, Membre-1 de la sous-famille A des transporteurs à cassette liant l'ATP, Muscles lisses vasculaires, Myocytes du muscle lisse, Néointima, Phosphatidylinositol 3-kinases, Protéines proto-oncogènes c-akt.
- pharmacologie : Agents protecteurs, Apolipoprotéine A-I, Lipoprotéines LDL.
- prévention et contrôle : Athérosclérose, Néointima.
- Animaux, Mâle, Rat Sprague-Dawley, Rats, Régulation de l'expression des gènes, Transduction du signal.
English descriptors
- KwdEn :
- AMP-Activated Protein Kinases (genetics), AMP-Activated Protein Kinases (metabolism), ATP Binding Cassette Transporter 1 (genetics), ATP Binding Cassette Transporter 1 (metabolism), Animals (MeSH), Aorta, Thoracic (cytology), Aorta, Thoracic (drug effects), Aorta, Thoracic (metabolism), Apolipoprotein A-I (pharmacology), Atherosclerosis (genetics), Atherosclerosis (metabolism), Atherosclerosis (pathology), Atherosclerosis (prevention & control), Cell Movement (drug effects), Cell Proliferation (drug effects), Gene Expression Regulation (MeSH), Heme Oxygenase-1 (genetics), Heme Oxygenase-1 (metabolism), Lipoproteins, LDL (antagonists & inhibitors), Lipoproteins, LDL (pharmacology), Male (MeSH), Muscle, Smooth, Vascular (cytology), Muscle, Smooth, Vascular (drug effects), Muscle, Smooth, Vascular (metabolism), Myocytes, Smooth Muscle (cytology), Myocytes, Smooth Muscle (drug effects), Myocytes, Smooth Muscle (metabolism), Neointima (genetics), Neointima (metabolism), Neointima (pathology), Neointima (prevention & control), Phosphatidylinositol 3-Kinases (genetics), Phosphatidylinositol 3-Kinases (metabolism), Protective Agents (pharmacology), Proto-Oncogene Proteins c-akt (genetics), Proto-Oncogene Proteins c-akt (metabolism), Rats (MeSH), Rats, Sprague-Dawley (MeSH), Signal Transduction (MeSH).
- MESH :
- chemical , antagonists & inhibitors : Lipoproteins, LDL.
- chemical , genetics : AMP-Activated Protein Kinases, ATP Binding Cassette Transporter 1, Heme Oxygenase-1, Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-akt.
- chemical , metabolism : AMP-Activated Protein Kinases, ATP Binding Cassette Transporter 1, Heme Oxygenase-1, Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-akt.
- cytology : Aorta, Thoracic, Muscle, Smooth, Vascular, Myocytes, Smooth Muscle.
- drug effects : Aorta, Thoracic, Cell Movement, Cell Proliferation, Muscle, Smooth, Vascular, Myocytes, Smooth Muscle.
- genetics : Atherosclerosis, Neointima.
- metabolism : Aorta, Thoracic, Atherosclerosis, Muscle, Smooth, Vascular, Myocytes, Smooth Muscle, Neointima.
- pathology : Atherosclerosis, Neointima.
- chemical , pharmacology : Apolipoprotein A-I, Lipoproteins, LDL, Protective Agents.
- prevention & control : Atherosclerosis, Neointima.
- Animals, Gene Expression Regulation, Male, Rats, Rats, Sprague-Dawley, Signal Transduction.
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
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en">The apolipoprotein A-I mimetic peptide, D-4F, restrains neointimal formation through heme oxygenase-1 up-regulation.</title>
<author><name sortKey="Liu, Donghui" sort="Liu, Donghui" uniqKey="Liu D" first="Donghui" last="Liu">Donghui Liu</name>
<affiliation wicri:level="1"><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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<author><name sortKey="Wu, Mengzhang" sort="Wu, Mengzhang" uniqKey="Wu M" first="Mengzhang" last="Wu">Mengzhang Wu</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>
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<affiliation wicri:level="3"><nlm:affiliation>Union Clinical Medical College of Fujian Medical University, Fuzhou, China.</nlm:affiliation>
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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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<author><name sortKey="Ding, Zhenzhen" sort="Ding, Zhenzhen" uniqKey="Ding Z" first="Zhenzhen" last="Ding">Zhenzhen Ding</name>
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<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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<affiliation wicri:level="3"><nlm:affiliation>Union Clinical Medical College of Fujian Medical University, Fuzhou, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Qian, Mingming" sort="Qian, Mingming" uniqKey="Qian M" first="Mingming" last="Qian">Mingming Qian</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>
</author>
<author><name sortKey="Tong, Zijia" sort="Tong, Zijia" uniqKey="Tong Z" first="Zijia" last="Tong">Zijia Tong</name>
<affiliation wicri:level="1"><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>
</affiliation>
<affiliation wicri:level="3"><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>
<placeName><settlement type="city">Fuzhou</settlement>
<region type="province">Fujian</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Xu, Wenqi" sort="Xu, Wenqi" uniqKey="Xu W" first="Wenqi" last="Xu">Wenqi Xu</name>
<affiliation wicri:level="1"><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>
<wicri:noRegion>Xiamen</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Zhang, Le" sort="Zhang, Le" uniqKey="Zhang L" first="Le" last="Zhang">Le Zhang</name>
<affiliation wicri:level="1"><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>
</affiliation>
</author>
<author><name sortKey="Chang, He" sort="Chang, He" uniqKey="Chang H" first="He" last="Chang">He Chang</name>
<affiliation wicri:level="1"><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>
</affiliation>
</author>
<author><name sortKey="Wang, Yan" sort="Wang, Yan" uniqKey="Wang Y" first="Yan" last="Wang">Yan Wang</name>
<affiliation wicri:level="1"><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>
</affiliation>
</author>
<author><name sortKey="Huang, Caihua" sort="Huang, Caihua" uniqKey="Huang C" first="Caihua" last="Huang">Caihua Huang</name>
<affiliation wicri:level="1"><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>
<wicri:noRegion>Xiamen</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Lin, Donghai" sort="Lin, Donghai" uniqKey="Lin D" first="Donghai" last="Lin">Donghai Lin</name>
<affiliation wicri:level="1"><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>
<wicri:noRegion>Xiamen</wicri:noRegion>
</affiliation>
</author>
</analytic>
<series><title level="j">Journal of cellular and molecular medicine</title>
<idno type="eISSN">1582-4934</idno>
<imprint><date when="2017" type="published">2017</date>
</imprint>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><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>
</textClass>
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<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>
<Author ValidYN="Y"><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>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Qian</LastName>
<ForeName>Mingming</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>
</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>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Wenqi</ForeName>
<Initials>W</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>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Le</ForeName>
<Initials>L</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>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>
<Initials>Y</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>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>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>08</Month>
<Day>02</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>J Cell Mol Med</MedlineTA>
<NlmUniqueID>101083777</NlmUniqueID>
<ISSNLinking>1582-1838</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C577834">ABCA1 protein, rat</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D064286">ATP Binding Cassette Transporter 1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016632">Apolipoprotein A-I</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C465468">D-4F peptide</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D008077">Lipoproteins, LDL</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D020011">Protective Agents</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C099252">oxidized low density lipoprotein</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 1.14.14.18</RegistryNumber>
<NameOfSubstance UI="D051547">Heme Oxygenase-1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.1.-</RegistryNumber>
<NameOfSubstance UI="D019869">Phosphatidylinositol 3-Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.31</RegistryNumber>
<NameOfSubstance UI="D055372">AMP-Activated Protein Kinases</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Front Pharmacol. 2017 Sep 29;8:708</RefSource>
<PMID Version="1">29033843</PMID>
</CommentsCorrections>
</CommentsCorrectionsList>
<MeshHeadingList><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>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<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>
</MeshHeading>
<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>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009131" MajorTopicYN="N">Muscle, Smooth, Vascular</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D032389" MajorTopicYN="N">Myocytes, Smooth Muscle</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="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>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019869" MajorTopicYN="N">Phosphatidylinositol 3-Kinases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020011" MajorTopicYN="N">Protective Agents</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<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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