Matricellular protein CCN3 mitigates abdominal aortic aneurysm
Identifieur interne : 003279 ( Ncbi/Curation ); précédent : 003278; suivant : 003280Matricellular protein CCN3 mitigates abdominal aortic aneurysm
Auteurs : Chao Zhang [États-Unis, République populaire de Chine] ; Dustin Van Der Voort [États-Unis] ; Hong Shi [États-Unis] ; Rongli Zhang [États-Unis] ; Yulan Qing [États-Unis] ; Shuichi Hiraoka [Japon] ; Minoru Takemoto [Japon] ; Koutaro Yokote [Japon] ; Joseph V. Moxon [Australie] ; Paul Norman [Australie] ; Laure Rittié [États-Unis] ; Helena Kuivaniemi [Afrique du Sud] ; G. Brandon Atkins [États-Unis] ; Stanton L. Gerson [États-Unis] ; Guo-Ping Shi [États-Unis] ; Jonathan Golledge [Australie] ; Nianguo Dong [République populaire de Chine] ; Bernard Perbal [France] ; Domenick A. Prosdocimo [États-Unis] ; Zhiyong Lin [États-Unis]Source :
- The Journal of Clinical Investigation [ 0021-9738 ] ; ????.
Abstract
Abdominal aortic aneurysm (AAA) is a major cause of morbidity and mortality; however, the mechanisms that are involved in disease initiation and progression are incompletely understood. Extracellular matrix proteins play an integral role in modulating vascular homeostasis in health and disease. Here, we determined that the expression of the matricellular protein CCN3 is strongly reduced in rodent AAA models, including angiotensin II–induced AAA and elastase perfusion–stimulated AAA. CCN3 levels were also reduced in human AAA biopsies compared with those in controls. In murine models of induced AAA, germline deletion of
Url:
DOI: 10.1172/JCI82337
PubMed: 26974158
PubMed Central: 4811126
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Matricellular protein CCN3 mitigates abdominal aortic aneurysm</title>
<author><name sortKey="Zhang, Chao" sort="Zhang, Chao" uniqKey="Zhang C" first="Chao" last="Zhang">Chao Zhang</name>
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<author><name sortKey="Van Der Voort, Dustin" sort="Van Der Voort, Dustin" uniqKey="Van Der Voort D" first="Dustin" last="Van Der Voort">Dustin Van Der Voort</name>
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<author><name sortKey="Moxon, Joseph V" sort="Moxon, Joseph V" uniqKey="Moxon J" first="Joseph V." last="Moxon">Joseph V. Moxon</name>
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<country xml:lang="fr" wicri:curation="lc">Australie</country>
<wicri:regionArea>The Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, School of Medicine and Dentistry, James Cook University, and The Department of Vascular and Endovascular Surgery, Townsville Hospital, Townsville, Queensland</wicri:regionArea>
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<author><name sortKey="Norman, Paul" sort="Norman, Paul" uniqKey="Norman P" first="Paul" last="Norman">Paul Norman</name>
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<author><name sortKey="Rittie, Laure" sort="Rittie, Laure" uniqKey="Rittie L" first="Laure" last="Rittié">Laure Rittié</name>
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<country xml:lang="fr" wicri:curation="lc">États-Unis</country>
<wicri:regionArea>Department of Dermatology, University of Michigan, Ann Arbor, Michigan</wicri:regionArea>
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<author><name sortKey="Kuivaniemi, Helena" sort="Kuivaniemi, Helena" uniqKey="Kuivaniemi H" first="Helena" last="Kuivaniemi">Helena Kuivaniemi</name>
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</affiliation>
</author>
<author><name sortKey="Atkins, G Brandon" sort="Atkins, G Brandon" uniqKey="Atkins G" first="G. Brandon" last="Atkins">G. Brandon Atkins</name>
<affiliation wicri:level="2"><nlm:aff id="A1">Case Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Harrington Heart and Vascular Institute, University Hospitals Case Medical Center, Cleveland, Ohio, USA.</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">États-Unis</country>
<wicri:regionArea>Case Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Harrington Heart and Vascular Institute, University Hospitals Case Medical Center, Cleveland, Ohio</wicri:regionArea>
<placeName><region type="state">Ohio</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Gerson, Stanton L" sort="Gerson, Stanton L" uniqKey="Gerson S" first="Stanton L." last="Gerson">Stanton L. Gerson</name>
<affiliation wicri:level="2"><nlm:aff id="A3">Division of Hematology and Oncology, University Hospitals Case Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA.</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">États-Unis</country>
<wicri:regionArea>Division of Hematology and Oncology, University Hospitals Case Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio</wicri:regionArea>
<placeName><region type="state">Ohio</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Shi, Guo Ping" sort="Shi, Guo Ping" uniqKey="Shi G" first="Guo-Ping" last="Shi">Guo-Ping Shi</name>
<affiliation wicri:level="2"><nlm:aff id="A10">Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA.</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">États-Unis</country>
<wicri:regionArea>Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Golledge, Jonathan" sort="Golledge, Jonathan" uniqKey="Golledge J" first="Jonathan" last="Golledge">Jonathan Golledge</name>
<affiliation wicri:level="1"><nlm:aff id="A6">The Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, School of Medicine and Dentistry, James Cook University, and The Department of Vascular and Endovascular Surgery, Townsville Hospital, Townsville, Queensland, Australia.</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">Australie</country>
<wicri:regionArea>The Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, School of Medicine and Dentistry, James Cook University, and The Department of Vascular and Endovascular Surgery, Townsville Hospital, Townsville, Queensland</wicri:regionArea>
<wicri:noRegion>Queensland</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Dong, Nianguo" sort="Dong, Nianguo" uniqKey="Dong N" first="Nianguo" last="Dong">Nianguo Dong</name>
<affiliation wicri:level="1"><nlm:aff id="A2">Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan</wicri:regionArea>
<wicri:noRegion>Wuhan</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Perbal, Bernard" sort="Perbal, Bernard" uniqKey="Perbal B" first="Bernard" last="Perbal">Bernard Perbal</name>
<affiliation wicri:level="3"><nlm:aff id="A11">University of Paris Diderot — Paris 7, Paris, France.</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">France</country>
<wicri:regionArea>University of Paris Diderot — Paris 7, Paris</wicri:regionArea>
<placeName><region type="region">Île-de-France</region>
<region type="old region">Île-de-France</region>
<settlement type="city">Paris</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Prosdocimo, Domenick A" sort="Prosdocimo, Domenick A" uniqKey="Prosdocimo D" first="Domenick A." last="Prosdocimo">Domenick A. Prosdocimo</name>
<affiliation wicri:level="2"><nlm:aff id="A1">Case Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Harrington Heart and Vascular Institute, University Hospitals Case Medical Center, Cleveland, Ohio, USA.</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">États-Unis</country>
<wicri:regionArea>Case Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Harrington Heart and Vascular Institute, University Hospitals Case Medical Center, Cleveland, Ohio</wicri:regionArea>
<placeName><region type="state">Ohio</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Lin, Zhiyong" sort="Lin, Zhiyong" uniqKey="Lin Z" first="Zhiyong" last="Lin">Zhiyong Lin</name>
<affiliation wicri:level="2"><nlm:aff id="A1">Case Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Harrington Heart and Vascular Institute, University Hospitals Case Medical Center, Cleveland, Ohio, USA.</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">États-Unis</country>
<wicri:regionArea>Case Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Harrington Heart and Vascular Institute, University Hospitals Case Medical Center, Cleveland, Ohio</wicri:regionArea>
<placeName><region type="state">Ohio</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j">The Journal of Clinical Investigation</title>
<idno type="ISSN">0021-9738</idno>
<idno type="eISSN">1558-8238</idno>
<imprint><date when="????">????</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>Abdominal aortic aneurysm (AAA) is a major cause of morbidity and mortality; however, the mechanisms that are involved in disease initiation and progression are incompletely understood. Extracellular matrix proteins play an integral role in modulating vascular homeostasis in health and disease. Here, we determined that the expression of the matricellular protein CCN3 is strongly reduced in rodent AAA models, including angiotensin II–induced AAA and elastase perfusion–stimulated AAA. CCN3 levels were also reduced in human AAA biopsies compared with those in controls. In murine models of induced AAA, germline deletion of <italic>Ccn3</italic>
resulted in severe phenotypes characterized by elastin fragmentation, vessel dilation, vascular inflammation, dissection, heightened ROS generation, and smooth muscle cell loss. Conversely, overexpression of CCN3 mitigated both elastase- and angiotensin II–induced AAA formation in mice. BM transplantation experiments suggested that the AAA phenotype of CCN3-deficient mice is intrinsic to the vasculature, as AAA was not exacerbated in WT animals that received CCN3-deficient BM and WT BM did not reduce AAA severity in CCN3-deficient mice. Genetic and pharmacological approaches implicated the ERK1/2 pathway as a critical regulator of CCN3-dependent AAA development. Together, these results demonstrate that CCN3 is a nodal regulator in AAA biology and identify CCN3 as a potential therapeutic target for vascular disease.</p>
</div>
</front>
</TEI>
</record>
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