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Nesfatin-1 functions as a switch for phenotype transformation and proliferation of VSMCs in hypertensive vascular remodeling
The phenotypic transformation from differentiated to dedifferentiated vascular smooth muscle cells (VSMCs) plays a crucial role in VSMC proliferation and vascular remodeling in many cardiovascular diseases including hypertension. Nesfatin-1, a multifunctional adipocytokine, is critically involved in...
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| Published in: | Biochimica et biophysica acta. Molecular basis of disease 2018-06, Vol.1864 (6), p.2154-2168 |
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| creator | Lu, Qing-Bo Wang, Hui-Ping Tang, Zi-Han Cheng, Han Du, Qiong Wang, Yuan-Ben Feng, Wu-Bing Li, Ke-Xue Cai, Wei-Wei Qiu, Li-Ying Sun, Hai-Jian |
| description | The phenotypic transformation from differentiated to dedifferentiated vascular smooth muscle cells (VSMCs) plays a crucial role in VSMC proliferation and vascular remodeling in many cardiovascular diseases including hypertension. Nesfatin-1, a multifunctional adipocytokine, is critically involved in the regulation of blood pressure. However, it is still largely unexplored whether nesfatin-1 is a potential candidate in VSMC phenotypic switch and proliferation in hypertension. Experiments were carried out in Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), human VSMCs and primary rat aortic VSMCs. We showed that the expression of nesfatin-1 was upregulated in media layer of the aorta in SHR and SHR-derived VSMCs. Nesfatin-1 promoted VSMC phenotypic transformation, accelerated cell cycle progression and proliferation. Knockdown of nesfatin-1 inhibited the VSMC phenotype switch from a contractile to a synthetic state, attenuated cell cycle progression and retarded VSMC proliferation in SHR-derived VSMCs. Moreover, nesfatin-1-activated PI3K/Akt/mTOR signaling was abolished by JAK/STAT inhibitor WP1066, and the increased phosphorylation levels of JAK2/STAT3 in response to nesfatin-1 were suppressed by inhibition of PI3K/Akt/mTOR in VSMCs. Pharmacological blockade of the forming feedback loop between PI3K/Akt/mTOR and JAK2/STAT3 prevented the proliferation of nesfatin-1-incubated VSMCs and primary VSMCs from SHR. Chronic intraperitoneal injection of nesfatin-1 caused severe hypertension and cardiovascular remodeling in normal rats. In contrast, silencing of nesfatin-1 gene ameliorated hypertension, phenotype switching, and vascular remodeling in the aorta of SHR. Therefore, our data identified nesfatin-1 as a key modulator in hypertension and vascular remodeling by facilitating VSMC phenotypic switching and proliferation.
[Display omitted]
•Nesfatin-1 promoted VSMC phenotypic transformation, cell cycle progression and proliferation.•PI3K/Akt/mTOR and JAK2/STAT formed a mutual transactivation loop in VSMCs response to nesfatin-1.•Chronic peripheral nesfatin-1 administration caused severe hypertension and cardiovascular remodeling in rats.•Silencing of nesfatin-1 gene ameliorated hypertension, phenotype switching, and vascular remodeling in the aorta of SHR. |
| doi_str_mv | 10.1016/j.bbadis.2018.04.002 |
| format | article |
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[Display omitted]
•Nesfatin-1 promoted VSMC phenotypic transformation, cell cycle progression and proliferation.•PI3K/Akt/mTOR and JAK2/STAT formed a mutual transactivation loop in VSMCs response to nesfatin-1.•Chronic peripheral nesfatin-1 administration caused severe hypertension and cardiovascular remodeling in rats.•Silencing of nesfatin-1 gene ameliorated hypertension, phenotype switching, and vascular remodeling in the aorta of SHR.</description><identifier>ISSN: 0925-4439</identifier><identifier>EISSN: 1879-260X</identifier><identifier>DOI: 10.1016/j.bbadis.2018.04.002</identifier><identifier>PMID: 29627363</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Aorta - cytology ; Blood Pressure - physiology ; Calcium-Binding Proteins - physiology ; Cell Proliferation ; Cells, Cultured ; Disease Models, Animal ; DNA-Binding Proteins - physiology ; Gene Knockdown Techniques ; Humans ; Hypertension ; Hypertension - etiology ; Hypertension - pathology ; Male ; Muscle, Smooth, Vascular - cytology ; Myocytes, Smooth Muscle - physiology ; Nerve Tissue Proteins - physiology ; Nesfatin-1 ; Phenotype ; Phenotypic transformation ; Primary Cell Culture ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; RNA, Small Interfering - metabolism ; Signal Transduction - physiology ; Vascular remodeling ; Vascular Remodeling - physiology ; VSMCs</subject><ispartof>Biochimica et biophysica acta. Molecular basis of disease, 2018-06, Vol.1864 (6), p.2154-2168</ispartof><rights>2018 Elsevier B.V.</rights><rights>Copyright © 2018 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-5a45f5b87ca1e5d75704823048178a6e3598a04fdaa43092013cd9d4d07656ac3</citedby><cites>FETCH-LOGICAL-c474t-5a45f5b87ca1e5d75704823048178a6e3598a04fdaa43092013cd9d4d07656ac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29627363$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Qing-Bo</creatorcontrib><creatorcontrib>Wang, Hui-Ping</creatorcontrib><creatorcontrib>Tang, Zi-Han</creatorcontrib><creatorcontrib>Cheng, Han</creatorcontrib><creatorcontrib>Du, Qiong</creatorcontrib><creatorcontrib>Wang, Yuan-Ben</creatorcontrib><creatorcontrib>Feng, Wu-Bing</creatorcontrib><creatorcontrib>Li, Ke-Xue</creatorcontrib><creatorcontrib>Cai, Wei-Wei</creatorcontrib><creatorcontrib>Qiu, Li-Ying</creatorcontrib><creatorcontrib>Sun, Hai-Jian</creatorcontrib><title>Nesfatin-1 functions as a switch for phenotype transformation and proliferation of VSMCs in hypertensive vascular remodeling</title><title>Biochimica et biophysica acta. Molecular basis of disease</title><addtitle>Biochim Biophys Acta Mol Basis Dis</addtitle><description>The phenotypic transformation from differentiated to dedifferentiated vascular smooth muscle cells (VSMCs) plays a crucial role in VSMC proliferation and vascular remodeling in many cardiovascular diseases including hypertension. Nesfatin-1, a multifunctional adipocytokine, is critically involved in the regulation of blood pressure. However, it is still largely unexplored whether nesfatin-1 is a potential candidate in VSMC phenotypic switch and proliferation in hypertension. Experiments were carried out in Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), human VSMCs and primary rat aortic VSMCs. We showed that the expression of nesfatin-1 was upregulated in media layer of the aorta in SHR and SHR-derived VSMCs. Nesfatin-1 promoted VSMC phenotypic transformation, accelerated cell cycle progression and proliferation. Knockdown of nesfatin-1 inhibited the VSMC phenotype switch from a contractile to a synthetic state, attenuated cell cycle progression and retarded VSMC proliferation in SHR-derived VSMCs. Moreover, nesfatin-1-activated PI3K/Akt/mTOR signaling was abolished by JAK/STAT inhibitor WP1066, and the increased phosphorylation levels of JAK2/STAT3 in response to nesfatin-1 were suppressed by inhibition of PI3K/Akt/mTOR in VSMCs. Pharmacological blockade of the forming feedback loop between PI3K/Akt/mTOR and JAK2/STAT3 prevented the proliferation of nesfatin-1-incubated VSMCs and primary VSMCs from SHR. Chronic intraperitoneal injection of nesfatin-1 caused severe hypertension and cardiovascular remodeling in normal rats. In contrast, silencing of nesfatin-1 gene ameliorated hypertension, phenotype switching, and vascular remodeling in the aorta of SHR. Therefore, our data identified nesfatin-1 as a key modulator in hypertension and vascular remodeling by facilitating VSMC phenotypic switching and proliferation.
[Display omitted]
•Nesfatin-1 promoted VSMC phenotypic transformation, cell cycle progression and proliferation.•PI3K/Akt/mTOR and JAK2/STAT formed a mutual transactivation loop in VSMCs response to nesfatin-1.•Chronic peripheral nesfatin-1 administration caused severe hypertension and cardiovascular remodeling in rats.•Silencing of nesfatin-1 gene ameliorated hypertension, phenotype switching, and vascular remodeling in the aorta of SHR.</description><subject>Animals</subject><subject>Aorta - cytology</subject><subject>Blood Pressure - physiology</subject><subject>Calcium-Binding Proteins - physiology</subject><subject>Cell Proliferation</subject><subject>Cells, Cultured</subject><subject>Disease Models, Animal</subject><subject>DNA-Binding Proteins - physiology</subject><subject>Gene Knockdown Techniques</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hypertension - etiology</subject><subject>Hypertension - pathology</subject><subject>Male</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Myocytes, Smooth Muscle - physiology</subject><subject>Nerve Tissue Proteins - physiology</subject><subject>Nesfatin-1</subject><subject>Phenotype</subject><subject>Phenotypic transformation</subject><subject>Primary Cell Culture</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Signal Transduction - physiology</subject><subject>Vascular remodeling</subject><subject>Vascular Remodeling - physiology</subject><subject>VSMCs</subject><issn>0925-4439</issn><issn>1879-260X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp9kE2PFCEQhonRuOPqPzCGo5duiwb642JiJrqarHrY1XgjDBQOk24YoXvMJv74ZdKrRwmBpPK8FPUQ8pJBzYC1bw71bqetz3UDrK9B1ADNI7JhfTdUTQs_HpMNDI2shODDBXmW8wHKajt4Si6aoW063vIN-fMFs9OzDxWjbglm9jFkqsum-befzZ66mOhxjyHOd0ekc9Ihl9KkzyTVwdJjiqN3mNZKdPT7zedtpj7QfUmkGUP2J6Qnnc0y6kQTTtHi6MPP5-SJ02PGFw_3Jfn24f3t9mN1_fXq0_bddWVEJ-ZKaiGd3PWd0Qyl7WQHom94OVjX6xa5HHoNwlmtBS8zA-PGDlZY6FrZasMvyev13fLVXwvmWU0-GxxHHTAuWTXQcAFSMCioWFGTYs4JnTomP-l0pxios3d1UKt3dfauQKjivcRePXRYdhPaf6G_ogvwdgWwzHnymFQ2HoNB6xOaWdno_9_hHujjl1A</recordid><startdate>201806</startdate><enddate>201806</enddate><creator>Lu, Qing-Bo</creator><creator>Wang, Hui-Ping</creator><creator>Tang, Zi-Han</creator><creator>Cheng, Han</creator><creator>Du, Qiong</creator><creator>Wang, Yuan-Ben</creator><creator>Feng, Wu-Bing</creator><creator>Li, Ke-Xue</creator><creator>Cai, Wei-Wei</creator><creator>Qiu, Li-Ying</creator><creator>Sun, Hai-Jian</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201806</creationdate><title>Nesfatin-1 functions as a switch for phenotype transformation and proliferation of VSMCs in hypertensive vascular remodeling</title><author>Lu, Qing-Bo ; Wang, Hui-Ping ; Tang, Zi-Han ; Cheng, Han ; Du, Qiong ; Wang, Yuan-Ben ; Feng, Wu-Bing ; Li, Ke-Xue ; Cai, Wei-Wei ; Qiu, Li-Ying ; Sun, Hai-Jian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-5a45f5b87ca1e5d75704823048178a6e3598a04fdaa43092013cd9d4d07656ac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Aorta - cytology</topic><topic>Blood Pressure - physiology</topic><topic>Calcium-Binding Proteins - physiology</topic><topic>Cell Proliferation</topic><topic>Cells, Cultured</topic><topic>Disease Models, Animal</topic><topic>DNA-Binding Proteins - physiology</topic><topic>Gene Knockdown Techniques</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Hypertension - etiology</topic><topic>Hypertension - pathology</topic><topic>Male</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Myocytes, Smooth Muscle - physiology</topic><topic>Nerve Tissue Proteins - physiology</topic><topic>Nesfatin-1</topic><topic>Phenotype</topic><topic>Phenotypic transformation</topic><topic>Primary Cell Culture</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Signal Transduction - physiology</topic><topic>Vascular remodeling</topic><topic>Vascular Remodeling - physiology</topic><topic>VSMCs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lu, Qing-Bo</creatorcontrib><creatorcontrib>Wang, Hui-Ping</creatorcontrib><creatorcontrib>Tang, Zi-Han</creatorcontrib><creatorcontrib>Cheng, Han</creatorcontrib><creatorcontrib>Du, Qiong</creatorcontrib><creatorcontrib>Wang, Yuan-Ben</creatorcontrib><creatorcontrib>Feng, Wu-Bing</creatorcontrib><creatorcontrib>Li, Ke-Xue</creatorcontrib><creatorcontrib>Cai, Wei-Wei</creatorcontrib><creatorcontrib>Qiu, Li-Ying</creatorcontrib><creatorcontrib>Sun, Hai-Jian</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochimica et biophysica acta. Molecular basis of disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lu, Qing-Bo</au><au>Wang, Hui-Ping</au><au>Tang, Zi-Han</au><au>Cheng, Han</au><au>Du, Qiong</au><au>Wang, Yuan-Ben</au><au>Feng, Wu-Bing</au><au>Li, Ke-Xue</au><au>Cai, Wei-Wei</au><au>Qiu, Li-Ying</au><au>Sun, Hai-Jian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nesfatin-1 functions as a switch for phenotype transformation and proliferation of VSMCs in hypertensive vascular remodeling</atitle><jtitle>Biochimica et biophysica acta. Molecular basis of disease</jtitle><addtitle>Biochim Biophys Acta Mol Basis Dis</addtitle><date>2018-06</date><risdate>2018</risdate><volume>1864</volume><issue>6</issue><spage>2154</spage><epage>2168</epage><pages>2154-2168</pages><issn>0925-4439</issn><eissn>1879-260X</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>The phenotypic transformation from differentiated to dedifferentiated vascular smooth muscle cells (VSMCs) plays a crucial role in VSMC proliferation and vascular remodeling in many cardiovascular diseases including hypertension. Nesfatin-1, a multifunctional adipocytokine, is critically involved in the regulation of blood pressure. However, it is still largely unexplored whether nesfatin-1 is a potential candidate in VSMC phenotypic switch and proliferation in hypertension. Experiments were carried out in Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), human VSMCs and primary rat aortic VSMCs. We showed that the expression of nesfatin-1 was upregulated in media layer of the aorta in SHR and SHR-derived VSMCs. Nesfatin-1 promoted VSMC phenotypic transformation, accelerated cell cycle progression and proliferation. Knockdown of nesfatin-1 inhibited the VSMC phenotype switch from a contractile to a synthetic state, attenuated cell cycle progression and retarded VSMC proliferation in SHR-derived VSMCs. Moreover, nesfatin-1-activated PI3K/Akt/mTOR signaling was abolished by JAK/STAT inhibitor WP1066, and the increased phosphorylation levels of JAK2/STAT3 in response to nesfatin-1 were suppressed by inhibition of PI3K/Akt/mTOR in VSMCs. Pharmacological blockade of the forming feedback loop between PI3K/Akt/mTOR and JAK2/STAT3 prevented the proliferation of nesfatin-1-incubated VSMCs and primary VSMCs from SHR. Chronic intraperitoneal injection of nesfatin-1 caused severe hypertension and cardiovascular remodeling in normal rats. In contrast, silencing of nesfatin-1 gene ameliorated hypertension, phenotype switching, and vascular remodeling in the aorta of SHR. Therefore, our data identified nesfatin-1 as a key modulator in hypertension and vascular remodeling by facilitating VSMC phenotypic switching and proliferation.
[Display omitted]
•Nesfatin-1 promoted VSMC phenotypic transformation, cell cycle progression and proliferation.•PI3K/Akt/mTOR and JAK2/STAT formed a mutual transactivation loop in VSMCs response to nesfatin-1.•Chronic peripheral nesfatin-1 administration caused severe hypertension and cardiovascular remodeling in rats.•Silencing of nesfatin-1 gene ameliorated hypertension, phenotype switching, and vascular remodeling in the aorta of SHR.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>29627363</pmid><doi>10.1016/j.bbadis.2018.04.002</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Aorta - cytology Blood Pressure - physiology Calcium-Binding Proteins - physiology Cell Proliferation Cells, Cultured Disease Models, Animal DNA-Binding Proteins - physiology Gene Knockdown Techniques Humans Hypertension Hypertension - etiology Hypertension - pathology Male Muscle, Smooth, Vascular - cytology Myocytes, Smooth Muscle - physiology Nerve Tissue Proteins - physiology Nesfatin-1 Phenotype Phenotypic transformation Primary Cell Culture Rats Rats, Inbred SHR Rats, Inbred WKY RNA, Small Interfering - metabolism Signal Transduction - physiology Vascular remodeling Vascular Remodeling - physiology VSMCs |
| title | Nesfatin-1 functions as a switch for phenotype transformation and proliferation of VSMCs in hypertensive vascular remodeling |
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