The inhibitor of autophagy SBI-0206965 aggravates atherosclerosis through decreasing myeloid-derived suppressor cells
Identifieur interne : 000522 ( Pmc/Curation ); précédent : 000521; suivant : 000523The inhibitor of autophagy SBI-0206965 aggravates atherosclerosis through decreasing myeloid-derived suppressor cells
Auteurs : Bo Wang [République populaire de Chine] ; Guanjun Dong [République populaire de Chine] ; Qingqiing Zhang [République populaire de Chine] ; Fenglian Yan [République populaire de Chine] ; Zhihua Li [République populaire de Chine] ; Chunxia Li [République populaire de Chine] ; Hui Zhang [République populaire de Chine] ; Qun Ma [République populaire de Chine] ; Jun Dai [République populaire de Chine] ; Chuanping Si [République populaire de Chine] ; Huabao Xiong [États-Unis]Source :
- Experimental and Therapeutic Medicine [ 1792-0981 ] ; 2019.
Abstract
Atherosclerosis (AS) is currently the leading cause of mortality worldwide, with the development of new strategies to prevent the formation and rupture of atherosclerotic plaques being a paramount area of research. Amounting evidence suggests autophagy has an important role in the pathogenesis of AS and may be a potential therapeutic target. In this study, the effect of SBI-0206965(6965), a novel inhibitor of autophagy, was tested on the development of AS in apolipoprotein E deficient (ApoE−/−) mice. Systemic application of 6965 was found to aggravate AS, with increased plaque size and decreased plaque stability in comparison with the control. Of note, it was observed that 6965 decreased the proportion of myeloid-derived suppressor cells (MDSCs). Further investigation demonstrated MDSCs markedly alleviated AS in ApoE−/− mice; while 6965 reduced the viability and promoted apoptosis of MDSCs
Url:
DOI: 10.3892/etm.2019.8317
PubMed: 32010311
PubMed Central: 6966176
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<series><title level="j">Experimental and Therapeutic Medicine</title>
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<front><div type="abstract" xml:lang="en"><p>Atherosclerosis (AS) is currently the leading cause of mortality worldwide, with the development of new strategies to prevent the formation and rupture of atherosclerotic plaques being a paramount area of research. Amounting evidence suggests autophagy has an important role in the pathogenesis of AS and may be a potential therapeutic target. In this study, the effect of SBI-0206965(6965), a novel inhibitor of autophagy, was tested on the development of AS in apolipoprotein E deficient (ApoE<sup>−/−</sup>
) mice. Systemic application of 6965 was found to aggravate AS, with increased plaque size and decreased plaque stability in comparison with the control. Of note, it was observed that 6965 decreased the proportion of myeloid-derived suppressor cells (MDSCs). Further investigation demonstrated MDSCs markedly alleviated AS in ApoE<sup>−/−</sup>
mice; while 6965 reduced the viability and promoted apoptosis of MDSCs <italic>in vitro</italic>
. This is the first study describing an association between autophagy and MDSCs in AS models, providing a novel mechanism to potentially target in the management of this condition.</p>
</div>
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<author><name sortKey="Layland, Le" uniqKey="Layland L">LE Layland</name>
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</TEI>
<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Exp Ther Med</journal-id>
<journal-id journal-id-type="iso-abbrev">Exp Ther Med</journal-id>
<journal-id journal-id-type="publisher-id">ETM</journal-id>
<journal-title-group><journal-title>Experimental and Therapeutic Medicine</journal-title>
</journal-title-group>
<issn pub-type="ppub">1792-0981</issn>
<issn pub-type="epub">1792-1015</issn>
<publisher><publisher-name>D.A. Spandidos</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">32010311</article-id>
<article-id pub-id-type="pmc">6966176</article-id>
<article-id pub-id-type="doi">10.3892/etm.2019.8317</article-id>
<article-id pub-id-type="publisher-id">ETM-0-0-8317</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Articles</subject>
</subj-group>
</article-categories>
<title-group><article-title>The inhibitor of autophagy SBI-0206965 aggravates atherosclerosis through decreasing myeloid-derived suppressor cells</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Wang</surname>
<given-names>Bo</given-names>
</name>
<xref ref-type="aff" rid="af1-etm-0-0-8317">1</xref>
<xref ref-type="aff" rid="af2-etm-0-0-8317">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Dong</surname>
<given-names>Guanjun</given-names>
</name>
<xref ref-type="aff" rid="af2-etm-0-0-8317">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zhang</surname>
<given-names>Qingqiing</given-names>
</name>
<xref ref-type="aff" rid="af2-etm-0-0-8317">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Yan</surname>
<given-names>Fenglian</given-names>
</name>
<xref ref-type="aff" rid="af2-etm-0-0-8317">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Li</surname>
<given-names>Zhihua</given-names>
</name>
<xref ref-type="aff" rid="af2-etm-0-0-8317">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Li</surname>
<given-names>Chunxia</given-names>
</name>
<xref ref-type="aff" rid="af2-etm-0-0-8317">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zhang</surname>
<given-names>Hui</given-names>
</name>
<xref ref-type="aff" rid="af2-etm-0-0-8317">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ma</surname>
<given-names>Qun</given-names>
</name>
<xref ref-type="aff" rid="af2-etm-0-0-8317">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Dai</surname>
<given-names>Jun</given-names>
</name>
<xref ref-type="aff" rid="af2-etm-0-0-8317">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Si</surname>
<given-names>Chuanping</given-names>
</name>
<xref ref-type="aff" rid="af2-etm-0-0-8317">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Xiong</surname>
<given-names>Huabao</given-names>
</name>
<xref ref-type="aff" rid="af3-etm-0-0-8317">3</xref>
<xref rid="c1-etm-0-0-8317" ref-type="corresp"></xref>
</contrib>
</contrib-group>
<aff id="af1-etm-0-0-8317"><label>1</label>
Institute of Forensic Medicine and Laboratory Medicine, Jining Medical University, Jining, Shandong 272067, P.R. China</aff>
<aff id="af2-etm-0-0-8317"><label>2</label>
Institute of Immunology and Molecular Medicine, Jining Medical University, Jining, Shandong 272067, P.R. China</aff>
<aff id="af3-etm-0-0-8317"><label>3</label>
Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA</aff>
<author-notes><corresp id="c1-etm-0-0-8317"><italic>Correspondence to</italic>
: Dr Huabao Xiong, Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA, E-mail: <email>huabao.xiong@mssm.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>2</month>
<year>2020</year>
</pub-date>
<pub-date pub-type="epub"><day>11</day>
<month>12</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>11</day>
<month>12</month>
<year>2019</year>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on the . </pmc-comment>
<volume>19</volume>
<issue>2</issue>
<fpage>1370</fpage>
<lpage>1378</lpage>
<history><date date-type="received"><day>19</day>
<month>4</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>14</day>
<month>11</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>Copyright: © Wang et al.</copyright-statement>
<copyright-year>2020</copyright-year>
<license license-type="open-access"><license-p>This is an open access article distributed under the terms of the <ext-link ext-link-type="uri" xlink:href="https://creativecommons.org/licenses/by-nc-nd/4.0/">Creative Commons Attribution-NonCommercial-NoDerivs License</ext-link>
, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.</license-p>
</license>
</permissions>
<abstract><p>Atherosclerosis (AS) is currently the leading cause of mortality worldwide, with the development of new strategies to prevent the formation and rupture of atherosclerotic plaques being a paramount area of research. Amounting evidence suggests autophagy has an important role in the pathogenesis of AS and may be a potential therapeutic target. In this study, the effect of SBI-0206965(6965), a novel inhibitor of autophagy, was tested on the development of AS in apolipoprotein E deficient (ApoE<sup>−/−</sup>
) mice. Systemic application of 6965 was found to aggravate AS, with increased plaque size and decreased plaque stability in comparison with the control. Of note, it was observed that 6965 decreased the proportion of myeloid-derived suppressor cells (MDSCs). Further investigation demonstrated MDSCs markedly alleviated AS in ApoE<sup>−/−</sup>
mice; while 6965 reduced the viability and promoted apoptosis of MDSCs <italic>in vitro</italic>
. This is the first study describing an association between autophagy and MDSCs in AS models, providing a novel mechanism to potentially target in the management of this condition.</p>
</abstract>
<kwd-group><kwd>autophagy</kwd>
<kwd>SBI-0206965</kwd>
<kwd>atherosclerosis</kwd>
<kwd>plaque stability</kwd>
<kwd>myeloid-derived suppressor cells</kwd>
</kwd-group>
</article-meta>
</front>
<floats-group><fig id="f1-etm-0-0-8317" orientation="portrait" position="float"><label>Figure 1.</label>
<caption><p>Treatment with 6965 promotes the development of atherosclerotic lesions independent of cholesterol levels. (A) Total plasma cholesterol and triglyceride levels of the control and 6965 groups. (B) Representative hematoxylin and eosin staining depicting the aortic roots from mice in the control and 6965-treated groups (magnification, ×20). Lesion area (µm<sup>2</sup>
) represents the sum of all the areas occupied by plaques in every pathological section. Total plaque area (%) represents the ratio of total plaque area to the cross-sectional area of the aortic root. Data are shown as the mean ± standard deviation. *P<0.05 and **P<0.01 vs. the control.</p>
</caption>
<graphic xlink:href="etm-19-02-1370-g00"></graphic>
</fig>
<fig id="f2-etm-0-0-8317" orientation="portrait" position="float"><label>Figure 2.</label>
<caption><p>Treatment with 6965 decreases plaque stability. Representative images of (A) macrophages, (B) smooth muscle cells and (C) apoptosis from the control and 6965-treated groups (magnification, ×40). Macrophage and SMC contents were analyzed through immunohistochemistry. TUNEL staining was used to detect apoptotic cells. Data are presented as the percentage of stained plaque areas in the entirety of the lesions. Data are shown as the mean ± standard deviation. *P<0.05 and **P<0.01 vs. the control. TUNEL, Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling; SMC, smooth muscle cell.</p>
</caption>
<graphic xlink:href="etm-19-02-1370-g01"></graphic>
</fig>
<fig id="f3-etm-0-0-8317" orientation="portrait" position="float"><label>Figure 3.</label>
<caption><p>Treatment with 6965 decreases the levels of MDSCs. (A) Flow cytometry and fluorescent staining were used to evaluate the proportions of CD11b<sup>+</sup>
Gr-1<sup>+</sup>
MDSCs. Representative images of the bone marrow, spleen and peripheral blood from different groups are shown. Data are presented as the mean ± SD. *P<0.05 and **P<0.01. (B) The expression of Gr-1 in plaques was analyzed by immunohistochemistry and the percentage of Gr-1 positive area was calculated in the total lesioned area (magnification, ×40). Data are shown as the mean ± SD. *P<0.05 vs. the control. SD, standard deviation; CD, cluster of differentiation; MDSCs, myeloid-derived suppressor cells.</p>
</caption>
<graphic xlink:href="etm-19-02-1370-g02"></graphic>
</fig>
<fig id="f4-etm-0-0-8317" orientation="portrait" position="float"><label>Figure 4.</label>
<caption><p>Adoptive transfer of MDSCs reduces atherosclerotic lesions in ApoE<sup>−/−</sup>
mice. (A) Representative images of oil red O-stained plaques in entire aortas (thoracic aorta and abdominal aorta) from the control and MDSC adoptive transfer groups (magnification, ×10). The black arrow indicates where the plaques are. (B) Representative cross-sections of lesions in the aortic valve area stained with hematoxylin and eosin are shown. Lesion area (µm<sup>2</sup>
) represents the sum of all the areas occupied by plaques in every pathological section (magnification, ×20). Total plaque area (%) represents the ratio of total plaque area to the cross-sectional area of the aortic root. Data are shown as the mean ± standard deviation. *P<0.05 vs. the control. MDSCs, myeloid-derived suppressor cells; ApoE<sup>−/−</sup>
, apolipoprotein E deficient.</p>
</caption>
<graphic xlink:href="etm-19-02-1370-g03"></graphic>
</fig>
<fig id="f5-etm-0-0-8317" orientation="portrait" position="float"><label>Figure 5.</label>
<caption><p>Treatment with 6965 decreases viability and increases apoptosis in oxLDL-stimulated MDSCs. (A) Cells were preincubated with 6965 (10 µM) for 30 min and then stimulated with 25 µg/ml oxLDL. Cell Counting Kit-8 assays were performed at different times after oxLDL stimulation to measure MSDC viability. (B) Flow cytometry detected MDSCs apoptosis. Data are shown as means ± standard deviation, calculated from triplicate experiments. *P<0.05 and ***P<0.001 vs. oxLDL. oxLDL, oxidized low density lipoprotein; MDSCs, myeloid-derived suppressor cells; PI, propidium iodide; OD, optical density.</p>
</caption>
<graphic xlink:href="etm-19-02-1370-g04"></graphic>
</fig>
</floats-group>
</pmc>
</record>
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