Prolactin protects cardiomyocytes against intermittent hypoxia-induced cell damage by the modulation of signaling pathways related to cardiac hypertrophy and proliferation.
Identifieur interne : 001506 ( Main/Exploration ); précédent : 001505; suivant : 001507Prolactin protects cardiomyocytes against intermittent hypoxia-induced cell damage by the modulation of signaling pathways related to cardiac hypertrophy and proliferation.
Auteurs : Dennis Jine-Yuan Hsieh [Taïwan] ; Chih-Yang Huang [Taïwan] ; Peiying Pai [Taïwan] ; Shyi-Gang P. Wang [Taïwan] ; Ying-Lan Tsai [Taïwan] ; Chia-Ning Li [Taïwan] ; Wei-Wen Kuo [Taïwan] ; Chih-Yang Huang [Taïwan]Source :
- International journal of cardiology [ 1874-1754 ] ; 2015.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Cardiomégalie (anatomopathologie), Cardiomégalie (métabolisme), Cardiomégalie (prévention et contrôle), Cardiotoniques (pharmacologie), Cardiotoniques (usage thérapeutique), Cellules cultivées (MeSH), Facteurs âges (MeSH), Hypoxie cellulaire (effets des médicaments et des substances chimiques), Hypoxie cellulaire (physiologie), Myocytes cardiaques (anatomopathologie), Myocytes cardiaques (effets des médicaments et des substances chimiques), Myocytes cardiaques (métabolisme), Mâle (MeSH), Prolactine (pharmacologie), Prolactine (usage thérapeutique), Prolifération cellulaire (effets des médicaments et des substances chimiques), Prolifération cellulaire (physiologie), Rat Sprague-Dawley (MeSH), Rats (MeSH), Transduction du signal (effets des médicaments et des substances chimiques), Transduction du signal (physiologie).
- MESH :
- anatomopathologie : Cardiomégalie, Myocytes cardiaques.
- effets des médicaments et des substances chimiques : Hypoxie cellulaire, Myocytes cardiaques, Prolifération cellulaire, Transduction du signal.
- métabolisme : Cardiomégalie, Myocytes cardiaques.
- pharmacologie : Cardiotoniques, Prolactine.
- physiologie : Hypoxie cellulaire, Prolifération cellulaire, Transduction du signal.
- prévention et contrôle : Cardiomégalie.
- usage thérapeutique : Cardiotoniques, Prolactine.
- Animaux, Cellules cultivées, Facteurs âges, Mâle, Rat Sprague-Dawley, Rats.
English descriptors
- KwdEn :
- Age Factors (MeSH), Animals (MeSH), Cardiomegaly (metabolism), Cardiomegaly (pathology), Cardiomegaly (prevention & control), Cardiotonic Agents (pharmacology), Cardiotonic Agents (therapeutic use), Cell Hypoxia (drug effects), Cell Hypoxia (physiology), Cell Proliferation (drug effects), Cell Proliferation (physiology), Cells, Cultured (MeSH), Male (MeSH), Myocytes, Cardiac (drug effects), Myocytes, Cardiac (metabolism), Myocytes, Cardiac (pathology), Prolactin (pharmacology), Prolactin (therapeutic use), Rats (MeSH), Rats, Sprague-Dawley (MeSH), Signal Transduction (drug effects), Signal Transduction (physiology).
- MESH :
- chemical , pharmacology : Cardiotonic Agents, Prolactin.
- drug effects : Cell Hypoxia, Cell Proliferation, Myocytes, Cardiac, Signal Transduction.
- metabolism : Cardiomegaly, Myocytes, Cardiac.
- pathology : Cardiomegaly, Myocytes, Cardiac.
- physiology : Cell Hypoxia, Cell Proliferation, Signal Transduction.
- prevention & control : Cardiomegaly.
- chemical , therapeutic use : Cardiotonic Agents, Prolactin.
- Age Factors, Animals, Cells, Cultured, Male, Rats, Rats, Sprague-Dawley.
Abstract
OBJECTIVES
Prolactin (PRL) is a multifunctional hormone that influences multiple physiological processes. It has been shown to have a protective effect on the cardiovascular system; however, the mechanisms of this effect are poorly understood. The purpose of the study was to elucidate the role of PRL in intermittent hypoxia (IH)-induced apoptosis in the cardiovascular system.
METHOD AND RESULTS
We established a hyperprolactinemic rat model by implanting two anterior pituitary (AP) glands into the renal capsule of male Sprague-Dawley rats. The rats were kept under normoxic conditions for 4weeks after implantation in order to reach the expression plateau of PRL in the plasma, and then treated with IH for 7 or 14days. Their hearts were then removed for histological and protein expression analyses. Cerebral cortex (CX)-grafted control rats challenged with IH displayed unique phenotypes such as a thicker heart wall, an abnormal myocardial architecture and an increased interstitial space of the left ventricle. They exhibited reduced expressions of p-JAK2, p-STAT5, cell cycle-dependent proteins (cyclin D1, cyclin E and cyclin A), IGF-IRα, PI3Kα, p-AKT and p-ERK1/2 in cardiomyocytes at 7days.
CONCLUSIONS
Our comprehensive analysis suggested that high plasma PRL can protect rat cardiomyocytes against IH through (1) the p-JAK2 and p-STAT5 pathways for transient cell proliferation, (2) the PI3Kα/AKT and MAPK survival pathways through IGF-I, and (3) the downregulation of IGF-II and ERK5, which inhibit cell hypertrophy.
DOI: 10.1016/j.ijcard.2014.11.154
PubMed: 25531577
Affiliations:
Links toward previous steps (curation, corpus...)
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Wang</name><affiliation wicri:level="1"><nlm:affiliation>Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan; Department of Physiology, National Yang-Ming University, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan; Department of Physiology, National Yang-Ming University, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Tsai, Ying Lan" sort="Tsai, Ying Lan" uniqKey="Tsai Y" first="Ying-Lan" last="Tsai">Ying-Lan Tsai</name><affiliation wicri:level="1"><nlm:affiliation>Athletic Training and Health Department, National Taiwan Sport University, Taoyuan 333, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Athletic Training and Health Department, National Taiwan Sport University, Taoyuan 333</wicri:regionArea><wicri:noRegion>Taoyuan 333</wicri:noRegion></affiliation></author><author><name sortKey="Li, Chia Ning" sort="Li, Chia Ning" uniqKey="Li C" first="Chia-Ning" last="Li">Chia-Ning Li</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung 402, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung 402</wicri:regionArea><wicri:noRegion>Taichung 402</wicri:noRegion></affiliation></author><author><name sortKey="Kuo, Wei Wen" sort="Kuo, Wei Wen" uniqKey="Kuo W" first="Wei-Wen" last="Kuo">Wei-Wen Kuo</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biological Science and Technology, China Medical University, Taichung, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Biological Science and Technology, China Medical University, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Huang, Chih Yang" sort="Huang, Chih Yang" uniqKey="Huang C" first="Chih-Yang" last="Huang">Chih-Yang Huang</name><affiliation wicri:level="1"><nlm:affiliation>Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan; Graduate Institute of Chinese Medical Science, China Medical University, Taichung, Taiwan; Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan. Electronic address: cyhuang@mail.cmu.edu.tw.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan; Graduate Institute of Chinese Medical Science, China Medical University, Taichung, Taiwan; Department of Health and Nutrition Biotechnology, Asia University, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:25531577</idno><idno type="pmid">25531577</idno><idno type="doi">10.1016/j.ijcard.2014.11.154</idno><idno type="wicri:Area/Main/Corpus">001726</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">001726</idno><idno type="wicri:Area/Main/Curation">001726</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">001726</idno><idno type="wicri:Area/Main/Exploration">001726</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Prolactin protects cardiomyocytes against intermittent hypoxia-induced cell damage by the modulation of signaling pathways related to cardiac hypertrophy and proliferation.</title><author><name sortKey="Hsieh, Dennis Jine Yuan" sort="Hsieh, Dennis Jine Yuan" uniqKey="Hsieh D" first="Dennis Jine-Yuan" last="Hsieh">Dennis Jine-Yuan Hsieh</name><affiliation wicri:level="1"><nlm:affiliation>School of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan; Clinical Laboratory, Chung Shan Medical University Hospital, Taichung 402, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>School of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan; Clinical Laboratory, Chung Shan Medical University Hospital, Taichung 402</wicri:regionArea><wicri:noRegion>Taichung 402</wicri:noRegion></affiliation></author><author><name sortKey="Huang, Chih Yang" sort="Huang, Chih Yang" uniqKey="Huang C" first="Chih-Yang" last="Huang">Chih-Yang Huang</name><affiliation wicri:level="1"><nlm:affiliation>Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Graduate Institute of Basic Medical Science, China Medical University, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Pai, Peiying" sort="Pai, Peiying" uniqKey="Pai P" first="Peiying" last="Pai">Peiying Pai</name><affiliation wicri:level="1"><nlm:affiliation>Division of Cardiology, China Medical University Hospital, Taichung, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Division of Cardiology, China Medical University Hospital, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Shyi Gang P" sort="Wang, Shyi Gang P" uniqKey="Wang S" first="Shyi-Gang P" last="Wang">Shyi-Gang P. Wang</name><affiliation wicri:level="1"><nlm:affiliation>Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan; Department of Physiology, National Yang-Ming University, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan; Department of Physiology, National Yang-Ming University, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Tsai, Ying Lan" sort="Tsai, Ying Lan" uniqKey="Tsai Y" first="Ying-Lan" last="Tsai">Ying-Lan Tsai</name><affiliation wicri:level="1"><nlm:affiliation>Athletic Training and Health Department, National Taiwan Sport University, Taoyuan 333, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Athletic Training and Health Department, National Taiwan Sport University, Taoyuan 333</wicri:regionArea><wicri:noRegion>Taoyuan 333</wicri:noRegion></affiliation></author><author><name sortKey="Li, Chia Ning" sort="Li, Chia Ning" uniqKey="Li C" first="Chia-Ning" last="Li">Chia-Ning Li</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung 402, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung 402</wicri:regionArea><wicri:noRegion>Taichung 402</wicri:noRegion></affiliation></author><author><name sortKey="Kuo, Wei Wen" sort="Kuo, Wei Wen" uniqKey="Kuo W" first="Wei-Wen" last="Kuo">Wei-Wen Kuo</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biological Science and Technology, China Medical University, Taichung, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Biological Science and Technology, China Medical University, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Huang, Chih Yang" sort="Huang, Chih Yang" uniqKey="Huang C" first="Chih-Yang" last="Huang">Chih-Yang Huang</name><affiliation wicri:level="1"><nlm:affiliation>Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan; Graduate Institute of Chinese Medical Science, China Medical University, Taichung, Taiwan; Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan. Electronic address: cyhuang@mail.cmu.edu.tw.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan; Graduate Institute of Chinese Medical Science, China Medical University, Taichung, Taiwan; Department of Health and Nutrition Biotechnology, Asia University, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author></analytic><series><title level="j">International journal of cardiology</title><idno type="eISSN">1874-1754</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Age Factors (MeSH)</term><term>Animals (MeSH)</term><term>Cardiomegaly (metabolism)</term><term>Cardiomegaly (pathology)</term><term>Cardiomegaly (prevention & control)</term><term>Cardiotonic Agents (pharmacology)</term><term>Cardiotonic Agents (therapeutic use)</term><term>Cell Hypoxia (drug effects)</term><term>Cell Hypoxia (physiology)</term><term>Cell Proliferation (drug effects)</term><term>Cell Proliferation (physiology)</term><term>Cells, Cultured (MeSH)</term><term>Male (MeSH)</term><term>Myocytes, Cardiac (drug effects)</term><term>Myocytes, Cardiac (metabolism)</term><term>Myocytes, Cardiac (pathology)</term><term>Prolactin (pharmacology)</term><term>Prolactin (therapeutic use)</term><term>Rats (MeSH)</term><term>Rats, Sprague-Dawley (MeSH)</term><term>Signal Transduction (drug effects)</term><term>Signal Transduction (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Cardiomégalie (anatomopathologie)</term><term>Cardiomégalie (métabolisme)</term><term>Cardiomégalie (prévention et contrôle)</term><term>Cardiotoniques (pharmacologie)</term><term>Cardiotoniques (usage thérapeutique)</term><term>Cellules cultivées (MeSH)</term><term>Facteurs âges (MeSH)</term><term>Hypoxie cellulaire (effets des médicaments et des substances chimiques)</term><term>Hypoxie cellulaire (physiologie)</term><term>Myocytes cardiaques (anatomopathologie)</term><term>Myocytes cardiaques (effets des médicaments et des substances chimiques)</term><term>Myocytes cardiaques (métabolisme)</term><term>Mâle (MeSH)</term><term>Prolactine (pharmacologie)</term><term>Prolactine (usage thérapeutique)</term><term>Prolifération cellulaire (effets des médicaments et des substances chimiques)</term><term>Prolifération cellulaire (physiologie)</term><term>Rat Sprague-Dawley (MeSH)</term><term>Rats (MeSH)</term><term>Transduction du signal (effets des médicaments et des substances chimiques)</term><term>Transduction du signal (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Cardiotonic Agents</term><term>Prolactin</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cardiomégalie</term><term>Myocytes cardiaques</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Hypoxia</term><term>Cell Proliferation</term><term>Myocytes, Cardiac</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Hypoxie cellulaire</term><term>Myocytes cardiaques</term><term>Prolifération cellulaire</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cardiomegaly</term><term>Myocytes, Cardiac</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cardiomégalie</term><term>Myocytes cardiaques</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cardiomegaly</term><term>Myocytes, Cardiac</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Cardiotoniques</term><term>Prolactine</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Hypoxie cellulaire</term><term>Prolifération cellulaire</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Hypoxia</term><term>Cell Proliferation</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Cardiomegaly</term></keywords><keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Cardiomégalie</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Cardiotonic Agents</term><term>Prolactin</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Cardiotoniques</term><term>Prolactine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Age Factors</term><term>Animals</term><term>Cells, Cultured</term><term>Male</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Facteurs âges</term><term>Mâle</term><term>Rat Sprague-Dawley</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>OBJECTIVES</b></p><p>Prolactin (PRL) is a multifunctional hormone that influences multiple physiological processes. It has been shown to have a protective effect on the cardiovascular system; however, the mechanisms of this effect are poorly understood. The purpose of the study was to elucidate the role of PRL in intermittent hypoxia (IH)-induced apoptosis in the cardiovascular system.</p></div><div type="abstract" xml:lang="en"><p><b>METHOD AND RESULTS</b></p><p>We established a hyperprolactinemic rat model by implanting two anterior pituitary (AP) glands into the renal capsule of male Sprague-Dawley rats. The rats were kept under normoxic conditions for 4weeks after implantation in order to reach the expression plateau of PRL in the plasma, and then treated with IH for 7 or 14days. Their hearts were then removed for histological and protein expression analyses. Cerebral cortex (CX)-grafted control rats challenged with IH displayed unique phenotypes such as a thicker heart wall, an abnormal myocardial architecture and an increased interstitial space of the left ventricle. They exhibited reduced expressions of p-JAK2, p-STAT5, cell cycle-dependent proteins (cyclin D1, cyclin E and cyclin A), IGF-IRα, PI3Kα, p-AKT and p-ERK1/2 in cardiomyocytes at 7days.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b></p><p>Our comprehensive analysis suggested that high plasma PRL can protect rat cardiomyocytes against IH through (1) the p-JAK2 and p-STAT5 pathways for transient cell proliferation, (2) the PI3Kα/AKT and MAPK survival pathways through IGF-I, and (3) the downregulation of IGF-II and ERK5, which inhibit cell hypertrophy.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25531577</PMID><DateCompleted><Year>2016</Year><Month>01</Month><Day>15</Day></DateCompleted><DateRevised><Year>2015</Year><Month>04</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1874-1754</ISSN><JournalIssue CitedMedium="Internet"><Volume>181</Volume><PubDate><Year>2015</Year><Month>Feb</Month><Day>15</Day></PubDate></JournalIssue><Title>International journal of cardiology</Title><ISOAbbreviation>Int J Cardiol</ISOAbbreviation></Journal><ArticleTitle>Prolactin protects cardiomyocytes against intermittent hypoxia-induced cell damage by the modulation of signaling pathways related to cardiac hypertrophy and proliferation.</ArticleTitle><Pagination><MedlinePgn>255-66</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ijcard.2014.11.154</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0167-5273(14)02326-2</ELocationID><Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">Prolactin (PRL) is a multifunctional hormone that influences multiple physiological processes. It has been shown to have a protective effect on the cardiovascular system; however, the mechanisms of this effect are poorly understood. The purpose of the study was to elucidate the role of PRL in intermittent hypoxia (IH)-induced apoptosis in the cardiovascular system.</AbstractText><AbstractText Label="METHOD AND RESULTS" NlmCategory="RESULTS">We established a hyperprolactinemic rat model by implanting two anterior pituitary (AP) glands into the renal capsule of male Sprague-Dawley rats. The rats were kept under normoxic conditions for 4weeks after implantation in order to reach the expression plateau of PRL in the plasma, and then treated with IH for 7 or 14days. Their hearts were then removed for histological and protein expression analyses. Cerebral cortex (CX)-grafted control rats challenged with IH displayed unique phenotypes such as a thicker heart wall, an abnormal myocardial architecture and an increased interstitial space of the left ventricle. They exhibited reduced expressions of p-JAK2, p-STAT5, cell cycle-dependent proteins (cyclin D1, cyclin E and cyclin A), IGF-IRα, PI3Kα, p-AKT and p-ERK1/2 in cardiomyocytes at 7days.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Our comprehensive analysis suggested that high plasma PRL can protect rat cardiomyocytes against IH through (1) the p-JAK2 and p-STAT5 pathways for transient cell proliferation, (2) the PI3Kα/AKT and MAPK survival pathways through IGF-I, and (3) the downregulation of IGF-II and ERK5, which inhibit cell hypertrophy.</AbstractText><CopyrightInformation>Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hsieh</LastName><ForeName>Dennis Jine-Yuan</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>School of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan; Clinical Laboratory, Chung Shan Medical University Hospital, Taichung 402, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Chih-Yang</ForeName><Initials>CY</Initials><AffiliationInfo><Affiliation>Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pai</LastName><ForeName>Peiying</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Division of Cardiology, China Medical University Hospital, Taichung, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Shyi-Gang P</ForeName><Initials>SG</Initials><AffiliationInfo><Affiliation>Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan; Department of Physiology, National Yang-Ming University, Taipei, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tsai</LastName><ForeName>Ying-Lan</ForeName><Initials>YL</Initials><AffiliationInfo><Affiliation>Athletic Training and Health Department, National Taiwan Sport University, Taoyuan 333, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Chia-Ning</ForeName><Initials>CN</Initials><AffiliationInfo><Affiliation>Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung 402, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kuo</LastName><ForeName>Wei-Wen</ForeName><Initials>WW</Initials><AffiliationInfo><Affiliation>Department of Biological Science and Technology, China Medical University, Taichung, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Chih-Yang</ForeName><Initials>CY</Initials><AffiliationInfo><Affiliation>Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan; Graduate Institute of Chinese Medical Science, China Medical University, Taichung, Taiwan; Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan. Electronic address: cyhuang@mail.cmu.edu.tw.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>11</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Int J Cardiol</MedlineTA><NlmUniqueID>8200291</NlmUniqueID><ISSNLinking>0167-5273</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002316">Cardiotonic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>9002-62-4</RegistryNumber><NameOfSubstance UI="D011388">Prolactin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000367" MajorTopicYN="N">Age Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006332" MajorTopicYN="N">Cardiomegaly</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002316" MajorTopicYN="N">Cardiotonic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015687" MajorTopicYN="N">Cell Hypoxia</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="N">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011388" MajorTopicYN="N">Prolactin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Apoptosis</Keyword><Keyword MajorTopicYN="N">Cardiomyocytes</Keyword><Keyword MajorTopicYN="N">Intermittent hypoxia</Keyword><Keyword MajorTopicYN="N">Normoxic</Keyword><Keyword MajorTopicYN="N">Prolactin</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>06</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2014</Year><Month>11</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>11</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>12</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>12</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>1</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25531577</ArticleId><ArticleId IdType="pii">S0167-5273(14)02326-2</ArticleId><ArticleId IdType="doi">10.1016/j.ijcard.2014.11.154</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Taïwan</li></country></list><tree><country name="Taïwan"><noRegion><name sortKey="Hsieh, Dennis Jine Yuan" sort="Hsieh, Dennis Jine Yuan" uniqKey="Hsieh D" first="Dennis Jine-Yuan" last="Hsieh">Dennis Jine-Yuan Hsieh</name></noRegion><name sortKey="Huang, Chih Yang" sort="Huang, Chih Yang" uniqKey="Huang C" first="Chih-Yang" last="Huang">Chih-Yang Huang</name><name sortKey="Huang, Chih Yang" sort="Huang, Chih Yang" uniqKey="Huang C" first="Chih-Yang" last="Huang">Chih-Yang Huang</name><name sortKey="Kuo, Wei Wen" sort="Kuo, Wei Wen" uniqKey="Kuo W" first="Wei-Wen" last="Kuo">Wei-Wen Kuo</name><name sortKey="Li, Chia Ning" sort="Li, Chia Ning" uniqKey="Li C" first="Chia-Ning" last="Li">Chia-Ning Li</name><name sortKey="Pai, Peiying" sort="Pai, Peiying" uniqKey="Pai P" first="Peiying" last="Pai">Peiying Pai</name><name sortKey="Tsai, Ying Lan" sort="Tsai, Ying Lan" uniqKey="Tsai Y" first="Ying-Lan" last="Tsai">Ying-Lan Tsai</name><name sortKey="Wang, Shyi Gang P" sort="Wang, Shyi Gang P" uniqKey="Wang S" first="Shyi-Gang P" last="Wang">Shyi-Gang P. 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