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Angiotensin II-induced Hypertension is Reduced by Deficiency of P-selectin Glycoprotein Ligand-1
Identification of inflammatory mediators that regulate the vascular response to vasopressor molecules may aid in the development of novel therapeutic agents to treat or prevent hypertensive vascular diseases. Leukocytes have recently been shown to be capable of modifying blood pressure responses to...
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| Published in: | Scientific reports 2018-02, Vol.8 (1), p.3223-7, Article 3223 |
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| creator | Wang, Qian Wang, Hui Wang, Jintao Venugopal, Jessica Kleiman, Kyle Guo, Chiao Sun, Yingxian Eitzman, Daniel T |
| description | Identification of inflammatory mediators that regulate the vascular response to vasopressor molecules may aid in the development of novel therapeutic agents to treat or prevent hypertensive vascular diseases. Leukocytes have recently been shown to be capable of modifying blood pressure responses to vasopressor molecules. The purpose of this study was to test the hypothesis that deficiency of the leukocyte ligand, Psgl-1, would reduce the pressor response to angiotensin II (Ang II). Mice deficient in Psgl-1 (Psgl-1
) along with wild-type (WT) controls were treated for 2 weeks with a continuous infusion of Ang II. No differences in blood pressure between the groups were noted at baseline, however after 5 days of Ang II infusion, systolic blood pressures were higher in WT compared to Psgl-1
mice. The pressor response to acute administration of high dose Ang II was also attenuated in Psgl-1
compared to WT mice. Chimeric mice with hematopoietic deficiency of Psgl-1 similarly showed a reduced pressor response to Ang II. This effect was associated with reduced plasma interleukin-17 (IL-17) levels in Psgl-1
mice and the reduced pressor response was restored by administration of recombinant IL-17. In conclusion, hematopoietic deficiency of Psgl-1 attenuates Ang II-induced hypertension, an effect that may be mediated by reduced IL-17. |
| doi_str_mv | 10.1038/s41598-018-21588-3 |
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) along with wild-type (WT) controls were treated for 2 weeks with a continuous infusion of Ang II. No differences in blood pressure between the groups were noted at baseline, however after 5 days of Ang II infusion, systolic blood pressures were higher in WT compared to Psgl-1
mice. The pressor response to acute administration of high dose Ang II was also attenuated in Psgl-1
compared to WT mice. Chimeric mice with hematopoietic deficiency of Psgl-1 similarly showed a reduced pressor response to Ang II. This effect was associated with reduced plasma interleukin-17 (IL-17) levels in Psgl-1
mice and the reduced pressor response was restored by administration of recombinant IL-17. In conclusion, hematopoietic deficiency of Psgl-1 attenuates Ang II-induced hypertension, an effect that may be mediated by reduced IL-17.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-018-21588-3</identifier><identifier>PMID: 29459637</identifier><language>eng</language><publisher>England: Nature Publishing Group</publisher><subject>Angiotensin ; Angiotensin II ; Blood pressure ; Circulatory system ; Hypertension ; Inflammation ; Interleukin 17 ; Leukocytes ; Ligands ; P-selectin ; P-selectin glycoprotein ligand 1 ; Vascular diseases</subject><ispartof>Scientific reports, 2018-02, Vol.8 (1), p.3223-7, Article 3223</ispartof><rights>2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c430t-d33b9a6e510960e860cc27ff58ce0aba11c72065edb3ebfa69d2b471e1c3566e3</citedby><cites>FETCH-LOGICAL-c430t-d33b9a6e510960e860cc27ff58ce0aba11c72065edb3ebfa69d2b471e1c3566e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2004118072/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2004118072?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,315,733,786,790,891,25783,27957,27958,37047,37048,44625,53827,53829,75483</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29459637$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Qian</creatorcontrib><creatorcontrib>Wang, Hui</creatorcontrib><creatorcontrib>Wang, Jintao</creatorcontrib><creatorcontrib>Venugopal, Jessica</creatorcontrib><creatorcontrib>Kleiman, Kyle</creatorcontrib><creatorcontrib>Guo, Chiao</creatorcontrib><creatorcontrib>Sun, Yingxian</creatorcontrib><creatorcontrib>Eitzman, Daniel T</creatorcontrib><title>Angiotensin II-induced Hypertension is Reduced by Deficiency of P-selectin Glycoprotein Ligand-1</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><description>Identification of inflammatory mediators that regulate the vascular response to vasopressor molecules may aid in the development of novel therapeutic agents to treat or prevent hypertensive vascular diseases. Leukocytes have recently been shown to be capable of modifying blood pressure responses to vasopressor molecules. The purpose of this study was to test the hypothesis that deficiency of the leukocyte ligand, Psgl-1, would reduce the pressor response to angiotensin II (Ang II). Mice deficient in Psgl-1 (Psgl-1
) along with wild-type (WT) controls were treated for 2 weeks with a continuous infusion of Ang II. No differences in blood pressure between the groups were noted at baseline, however after 5 days of Ang II infusion, systolic blood pressures were higher in WT compared to Psgl-1
mice. The pressor response to acute administration of high dose Ang II was also attenuated in Psgl-1
compared to WT mice. Chimeric mice with hematopoietic deficiency of Psgl-1 similarly showed a reduced pressor response to Ang II. This effect was associated with reduced plasma interleukin-17 (IL-17) levels in Psgl-1
mice and the reduced pressor response was restored by administration of recombinant IL-17. In conclusion, hematopoietic deficiency of Psgl-1 attenuates Ang II-induced hypertension, an effect that may be mediated by reduced IL-17.</description><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Blood pressure</subject><subject>Circulatory system</subject><subject>Hypertension</subject><subject>Inflammation</subject><subject>Interleukin 17</subject><subject>Leukocytes</subject><subject>Ligands</subject><subject>P-selectin</subject><subject>P-selectin glycoprotein ligand 1</subject><subject>Vascular diseases</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNpdkUFr3DAQhUVpSUKaP5BDMfTSi1qNZMnypRDSNFlYaAnpWZXl8VbBK20lu-B_HyWbhiS6jGb0vYeGR8gpsM_AhP6Sa5Ctpgw05SC1puINOeKslpQLzt8-ux-Sk5xvWTmStzW0B-SwVNkq0RyR32dh4-OEIftQrVbUh3522FdXyw7TwziGyufqGvfzbqm-4eCdx-CWKg7VT5pxRDcV-eW4uLhLxa00a7-xoafwnrwb7Jjx5LEek1_fL27Or-j6x-Xq_GxNXS3YRHshutYqlMBaxVAr5hxvhkFqh8x2FsA1nCmJfSewG6xqe97VDSA4IZVCcUy-7n13c7fF3mGYkh3NLvmtTYuJ1puXL8H_MZv4z0gNWtWqGHx6NEjx74x5MlufHY6jDRjnbDhjDUArRFPQj6_Q2zinUNa7p2oAzRpeKL6nXIo5JxyePgPM3Gdo9hmakqF5yNCIIvrwfI0nyf_ExB1AU5f9</recordid><startdate>20180219</startdate><enddate>20180219</enddate><creator>Wang, Qian</creator><creator>Wang, Hui</creator><creator>Wang, Jintao</creator><creator>Venugopal, Jessica</creator><creator>Kleiman, Kyle</creator><creator>Guo, Chiao</creator><creator>Sun, Yingxian</creator><creator>Eitzman, Daniel T</creator><general>Nature Publishing Group</general><general>Nature Publishing Group UK</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180219</creationdate><title>Angiotensin II-induced Hypertension is Reduced by Deficiency of P-selectin Glycoprotein Ligand-1</title><author>Wang, Qian ; Wang, Hui ; Wang, Jintao ; Venugopal, Jessica ; Kleiman, Kyle ; Guo, Chiao ; Sun, Yingxian ; Eitzman, Daniel T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c430t-d33b9a6e510960e860cc27ff58ce0aba11c72065edb3ebfa69d2b471e1c3566e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Blood pressure</topic><topic>Circulatory system</topic><topic>Hypertension</topic><topic>Inflammation</topic><topic>Interleukin 17</topic><topic>Leukocytes</topic><topic>Ligands</topic><topic>P-selectin</topic><topic>P-selectin glycoprotein ligand 1</topic><topic>Vascular diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Qian</creatorcontrib><creatorcontrib>Wang, Hui</creatorcontrib><creatorcontrib>Wang, Jintao</creatorcontrib><creatorcontrib>Venugopal, Jessica</creatorcontrib><creatorcontrib>Kleiman, Kyle</creatorcontrib><creatorcontrib>Guo, Chiao</creatorcontrib><creatorcontrib>Sun, Yingxian</creatorcontrib><creatorcontrib>Eitzman, Daniel T</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Science Journals</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Qian</au><au>Wang, Hui</au><au>Wang, Jintao</au><au>Venugopal, Jessica</au><au>Kleiman, Kyle</au><au>Guo, Chiao</au><au>Sun, Yingxian</au><au>Eitzman, Daniel T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiotensin II-induced Hypertension is Reduced by Deficiency of P-selectin Glycoprotein Ligand-1</atitle><jtitle>Scientific reports</jtitle><addtitle>Sci Rep</addtitle><date>2018-02-19</date><risdate>2018</risdate><volume>8</volume><issue>1</issue><spage>3223</spage><epage>7</epage><pages>3223-7</pages><artnum>3223</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Identification of inflammatory mediators that regulate the vascular response to vasopressor molecules may aid in the development of novel therapeutic agents to treat or prevent hypertensive vascular diseases. Leukocytes have recently been shown to be capable of modifying blood pressure responses to vasopressor molecules. The purpose of this study was to test the hypothesis that deficiency of the leukocyte ligand, Psgl-1, would reduce the pressor response to angiotensin II (Ang II). Mice deficient in Psgl-1 (Psgl-1
) along with wild-type (WT) controls were treated for 2 weeks with a continuous infusion of Ang II. No differences in blood pressure between the groups were noted at baseline, however after 5 days of Ang II infusion, systolic blood pressures were higher in WT compared to Psgl-1
mice. The pressor response to acute administration of high dose Ang II was also attenuated in Psgl-1
compared to WT mice. Chimeric mice with hematopoietic deficiency of Psgl-1 similarly showed a reduced pressor response to Ang II. This effect was associated with reduced plasma interleukin-17 (IL-17) levels in Psgl-1
mice and the reduced pressor response was restored by administration of recombinant IL-17. In conclusion, hematopoietic deficiency of Psgl-1 attenuates Ang II-induced hypertension, an effect that may be mediated by reduced IL-17.</abstract><cop>England</cop><pub>Nature Publishing Group</pub><pmid>29459637</pmid><doi>10.1038/s41598-018-21588-3</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | Nature Open Access; Publicly Available Content Database; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Angiotensin Angiotensin II Blood pressure Circulatory system Hypertension Inflammation Interleukin 17 Leukocytes Ligands P-selectin P-selectin glycoprotein ligand 1 Vascular diseases |
| title | Angiotensin II-induced Hypertension is Reduced by Deficiency of P-selectin Glycoprotein Ligand-1 |
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