NPS2390, a Selective Calcium-sensing Receptor Antagonist Controls the Phenotypic Modulation of Hypoxic Human Pulmonary Arterial Smooth Muscle Cells by Regulating Autophagy
Identifieur interne : 000683 ( Pmc/Curation ); précédent : 000682; suivant : 000684NPS2390, a Selective Calcium-sensing Receptor Antagonist Controls the Phenotypic Modulation of Hypoxic Human Pulmonary Arterial Smooth Muscle Cells by Regulating Autophagy
Auteurs : Xue Peng [République populaire de Chine] ; Can Wei [République populaire de Chine] ; Hong-Zhu Li [République populaire de Chine] ; Hong-Xia Li [République populaire de Chine] ; Shu-Zhi Bai [République populaire de Chine] ; Li-Na Wang [République populaire de Chine] ; Yu-Hui Xi [République populaire de Chine] ; Jin Yan [République populaire de Chine] ; Chang-Qing Xu [République populaire de Chine]Source :
- Journal of Translational Internal Medicine [ 2450-131X ] ; 2019.
Abstract
Calcium-sensing receptor (CaSR) is known to regulate hypoxia-induced pulmonary hypertension (HPH) and vascular remodeling via the phenotypic modulation of pulmonary arterial smooth muscle cells (PASMCs) in small pulmonary arteries. Moreover, autophagy is an essential modulator of VSMC phenotype. But it is not clear whether CaSR can regulate autophagy involving the phenotypic modulation under hypoxia.
The viability of human PASMCs was detected by cell cycle and BrdU. The expressions of proliferation protein, phenotypic marker protein, and autophagy protein in human PASMCs were determined by western blot.
Our results showed that hypoxia-induced autophagy was considerable at 24 h. The addition of NPS2390 decreased the expression of autophagy protein and synthetic phenotype marker protein osteopontin and increased the expression of contractile phenotype marker protein SMA-ɑ and calponin via suppressing downstream PI3K/Akt/mTOR signal pathways.
Our study demonstrates that treatment of NPS2390 was conducive to inhibit the proliferation and reverse phenotypic modulation of PASMCs by regulating autophagy levels.
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DOI: 10.2478/jtim-2019-0013
PubMed: 31380238
PubMed Central: 6661874
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country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Li, Hong Xia" sort="Li, Hong Xia" uniqKey="Li H" first="Hong-Xia" last="Li">Hong-Xia Li</name><affiliation wicri:level="1"><nlm:aff id="j_jtim-2019-0013_aff_001"><institution>Department of Pathophysiology, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Bai, Shu Zhi" sort="Bai, Shu Zhi" uniqKey="Bai S" first="Shu-Zhi" last="Bai">Shu-Zhi Bai</name><affiliation wicri:level="1"><nlm:aff id="j_jtim-2019-0013_aff_001"><institution>Department of Pathophysiology, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang 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Heilongjiang Province,<country country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Yan, Jin" sort="Yan, Jin" uniqKey="Yan J" first="Jin" last="Yan">Jin Yan</name><affiliation wicri:level="1"><nlm:aff id="j_jtim-2019-0013_aff_003"><institution>Laboratory of Medical Genetics, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Xu, Chang Qing" sort="Xu, Chang Qing" uniqKey="Xu C" first="Chang-Qing" last="Xu">Chang-Qing Xu</name><affiliation wicri:level="1"><nlm:aff id="j_jtim-2019-0013_aff_001"><institution>Department of Pathophysiology, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="j_jtim-2019-0013_aff_004"><institution>Bio-pharmaceutical Key Laboratory of Heilongjiang Province</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31380238</idno><idno type="pmc">6661874</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6661874</idno><idno type="RBID">PMC:6661874</idno><idno type="doi">10.2478/jtim-2019-0013</idno><date when="2019">2019</date><idno 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strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="j_jtim-2019-0013_aff_002"><institution>Department of Forensic Medicine, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Wei, Can" sort="Wei, Can" uniqKey="Wei C" first="Can" last="Wei">Can Wei</name><affiliation wicri:level="1"><nlm:aff id="j_jtim-2019-0013_aff_001"><institution>Department of Pathophysiology, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Li, Hong Zhu" sort="Li, Hong Zhu" uniqKey="Li H" first="Hong-Zhu" last="Li">Hong-Zhu Li</name><affiliation wicri:level="1"><nlm:aff id="j_jtim-2019-0013_aff_001"><institution>Department of Pathophysiology, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Li, Hong Xia" sort="Li, Hong Xia" uniqKey="Li H" first="Hong-Xia" last="Li">Hong-Xia Li</name><affiliation wicri:level="1"><nlm:aff id="j_jtim-2019-0013_aff_001"><institution>Department of Pathophysiology, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Bai, Shu Zhi" sort="Bai, Shu Zhi" uniqKey="Bai S" first="Shu-Zhi" last="Bai">Shu-Zhi Bai</name><affiliation wicri:level="1"><nlm:aff id="j_jtim-2019-0013_aff_001"><institution>Department of Pathophysiology, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Wang, Li Na" sort="Wang, Li Na" uniqKey="Wang L" first="Li-Na" last="Wang">Li-Na Wang</name><affiliation wicri:level="1"><nlm:aff id="j_jtim-2019-0013_aff_001"><institution>Department of Pathophysiology, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Xi, Yu Hui" sort="Xi, Yu Hui" uniqKey="Xi Y" first="Yu-Hui" last="Xi">Yu-Hui Xi</name><affiliation wicri:level="1"><nlm:aff id="j_jtim-2019-0013_aff_001"><institution>Department of Pathophysiology, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Yan, Jin" sort="Yan, Jin" uniqKey="Yan J" first="Jin" last="Yan">Jin Yan</name><affiliation wicri:level="1"><nlm:aff id="j_jtim-2019-0013_aff_003"><institution>Laboratory of Medical Genetics, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Xu, Chang Qing" sort="Xu, Chang Qing" uniqKey="Xu C" first="Chang-Qing" last="Xu">Chang-Qing Xu</name><affiliation wicri:level="1"><nlm:aff id="j_jtim-2019-0013_aff_001"><institution>Department of Pathophysiology, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="j_jtim-2019-0013_aff_004"><institution>Bio-pharmaceutical Key Laboratory of Heilongjiang Province</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></analytic><series><title level="j">Journal of Translational Internal Medicine</title><idno type="ISSN">2450-131X</idno><idno type="eISSN">2224-4018</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>Abstract</title><sec id="j_jtim-2019-0013_s_005"><title>Background and Objectives</title><p>Calcium-sensing receptor (CaSR) is known to regulate hypoxia-induced pulmonary hypertension (HPH) and vascular remodeling via the phenotypic modulation of pulmonary arterial smooth muscle cells (PASMCs) in small pulmonary arteries. Moreover, autophagy is an essential modulator of VSMC phenotype. But it is not clear whether CaSR can regulate autophagy involving the phenotypic modulation under hypoxia.</p></sec><sec id="j_jtim-2019-0013_s_006"><title>Methods</title><p>The viability of human PASMCs was detected by cell cycle and BrdU. The expressions of proliferation protein, phenotypic marker protein, and autophagy protein in human PASMCs were determined by western blot.</p></sec><sec id="j_jtim-2019-0013_s_007"><title>Results</title><p>Our results showed that hypoxia-induced autophagy was considerable at 24 h. The addition of NPS2390 decreased the expression of autophagy protein and synthetic phenotype marker protein osteopontin and increased the expression of contractile phenotype marker protein SMA-ɑ and calponin via suppressing downstream PI3K/Akt/mTOR signal pathways.</p></sec><sec id="j_jtim-2019-0013_s_008"><title>Conclusions</title><p>Our study demonstrates that treatment of NPS2390 was conducive to inhibit the proliferation and reverse phenotypic modulation of PASMCs by regulating autophagy levels.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Mizushima, N" uniqKey="Mizushima N">N Mizushima</name></author><author><name sortKey="Komatsu, M" uniqKey="Komatsu M">M Komatsu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Klionsky, Dj" uniqKey="Klionsky D">DJ Klionsky</name></author><author><name sortKey="Abdalla, Fc" uniqKey="Abdalla F">FC Abdalla</name></author><author><name 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<front><journal-meta><journal-id journal-id-type="nlm-ta">J Transl Int Med</journal-id><journal-id journal-id-type="iso-abbrev">J Transl Int Med</journal-id><journal-id journal-id-type="publisher-id">jtim</journal-id><journal-id journal-id-type="pmc">jtim</journal-id><journal-title-group><journal-title>Journal of Translational Internal Medicine</journal-title></journal-title-group><issn pub-type="ppub">2450-131X</issn><issn pub-type="epub">2224-4018</issn><publisher><publisher-name>Sciendo</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31380238</article-id><article-id pub-id-type="pmc">6661874</article-id><article-id pub-id-type="publisher-id">jtim-2019-0013</article-id><article-id pub-id-type="doi">10.2478/jtim-2019-0013</article-id><article-categories><subj-group subj-group-type="heading"><subject>Original Article</subject></subj-group></article-categories><title-group><article-title>NPS2390, a Selective Calcium-sensing Receptor Antagonist Controls the Phenotypic Modulation of Hypoxic Human Pulmonary Arterial Smooth Muscle Cells by Regulating Autophagy</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Peng</surname><given-names>Xue</given-names></name><xref ref-type="aff" rid="j_jtim-2019-0013_aff_001"><sup>1</sup></xref><xref ref-type="aff" rid="j_jtim-2019-0013_aff_002"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Wei</surname><given-names>Can</given-names></name><xref ref-type="aff" rid="j_jtim-2019-0013_aff_001"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Li</surname><given-names>Hong-Zhu</given-names></name><xref ref-type="aff" rid="j_jtim-2019-0013_aff_001"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Li</surname><given-names>Hong-Xia</given-names></name><xref ref-type="aff" rid="j_jtim-2019-0013_aff_001"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Bai</surname><given-names>Shu-Zhi</given-names></name><xref ref-type="aff" rid="j_jtim-2019-0013_aff_001"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Li-Na</given-names></name><xref ref-type="aff" rid="j_jtim-2019-0013_aff_001"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Xi</surname><given-names>Yu-Hui</given-names></name><xref ref-type="aff" rid="j_jtim-2019-0013_aff_001"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Yan</surname><given-names>Jin</given-names></name><xref ref-type="aff" rid="j_jtim-2019-0013_aff_003"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>Xu</surname><given-names>Chang-Qing</given-names><prefix>Dr.</prefix></name><degrees>PhD</degrees><xref ref-type="corresp" rid="jtim-2019-0013_cor_001">*</xref><xref ref-type="aff" rid="j_jtim-2019-0013_aff_001"><sup>1</sup></xref><xref ref-type="aff" rid="j_jtim-2019-0013_aff_004"><sup>4</sup></xref></contrib><aff id="j_jtim-2019-0013_aff_001"><label>1</label><institution>Department of Pathophysiology, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></aff><aff id="j_jtim-2019-0013_aff_002"><label>2</label><institution>Department of Forensic Medicine, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></aff><aff id="j_jtim-2019-0013_aff_003"><label>3</label><institution>Laboratory of Medical Genetics, Harbin Medical University</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></aff><aff id="j_jtim-2019-0013_aff_004"><label>4</label><institution>Bio-pharmaceutical Key Laboratory of Heilongjiang Province</institution>,<city>Harbin</city>, Heilongjiang Province,<country country="CN">China</country></aff></contrib-group><author-notes><corresp id="jtim-2019-0013_cor_001"><label>*</label> Dr. Chang-Qing Xu, PhD, Department of Pathophysiology, Harbin Medical University, Harbin 150086, Heilongjiang Province, China <email xlink:href="mailto:xucq45@126.com">xucq45@126.com</email></corresp></author-notes><pub-date pub-type="collection"><month>6</month><year>2019</year></pub-date><pub-date pub-type="epub"><day>11</day><month>7</month><year>2019</year></pub-date><volume>7</volume><issue>2</issue><fpage>59</fpage><lpage>68</lpage><permissions><copyright-statement>© 2019 Xue Peng, Can Wei, Hong-Zhu Li, Hong-Xia Li, Shu-Zhi Bai, Li-Na Wang, Yu-Hui Xi, Jin Yan, Chang-Qing Xu, published by Sciendo</copyright-statement><copyright-year>2019</copyright-year><copyright-holder>Xue Peng, Can Wei, Hong-Zhu Li, Hong-Xia Li, Shu-Zhi Bai, Li-Na Wang, Yu-Hui Xi, Jin Yan, Chang-Qing Xu, published by Sciendo</copyright-holder><license license-type="open-access" specific-use="rights-object-archive-dnb" xlink:href="http://creativecommons.org/licenses/by-nc-nd/3.0"><license-p>This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.</license-p></license></permissions><abstract><title>Abstract</title><sec id="j_jtim-2019-0013_s_005"><title>Background and Objectives</title><p>Calcium-sensing receptor (CaSR) is known to regulate hypoxia-induced pulmonary hypertension (HPH) and vascular remodeling via the phenotypic modulation of pulmonary arterial smooth muscle cells (PASMCs) in small pulmonary arteries. Moreover, autophagy is an essential modulator of VSMC phenotype. But it is not clear whether CaSR can regulate autophagy involving the phenotypic modulation under hypoxia.</p></sec><sec id="j_jtim-2019-0013_s_006"><title>Methods</title><p>The viability of human PASMCs was detected by cell cycle and BrdU. The expressions of proliferation protein, phenotypic marker protein, and autophagy protein in human PASMCs were determined by western blot.</p></sec><sec id="j_jtim-2019-0013_s_007"><title>Results</title><p>Our results showed that hypoxia-induced autophagy was considerable at 24 h. The addition of NPS2390 decreased the expression of autophagy protein and synthetic phenotype marker protein osteopontin and increased the expression of contractile phenotype marker protein SMA-ɑ and calponin via suppressing downstream PI3K/Akt/mTOR signal pathways.</p></sec><sec id="j_jtim-2019-0013_s_008"><title>Conclusions</title><p>Our study demonstrates that treatment of NPS2390 was conducive to inhibit the proliferation and reverse phenotypic modulation of PASMCs by regulating autophagy levels.</p></sec></abstract><kwd-group><title>Key words</title><kwd>NPS2390</kwd><kwd>calcium-sensing receptors</kwd><kwd>hypoxia</kwd><kwd>pulmonary arterial smooth muscle cells</kwd><kwd>phenotypic modulation</kwd><kwd>autophagy</kwd></kwd-group><counts><page-count count="10"></page-count></counts></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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