Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts
Urotensin II (UII) contributes to cardiovascular diseases by activating vasoactive peptides. The present study aimed to determine the effect of UII on aldosterone (ALD) and its receptor in cultured adventitial fibroblasts (AFs) and the tunica adventitia of rat vessels to explore the possible mechani...
Gespeichert in:
| Veröffentlicht in: | Molecular medicine reports 2018-02, Vol.17 (2), p.2921-2928 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2928 |
|---|---|
| container_issue | 2 |
| container_start_page | 2921 |
| container_title | Molecular medicine reports |
| container_volume | 17 |
| creator | Li, Jun Zhang, Yong-Gang Luo, Li-Min Dong, Xiao Ding, Wen-Hui Dang, Shu-Yi |
| description | Urotensin II (UII) contributes to cardiovascular diseases by activating vasoactive peptides. The present study aimed to determine the effect of UII on aldosterone (ALD) and its receptor in cultured adventitial fibroblasts (AFs) and the tunica adventitia of rat vessels to explore the possible mechanisms underlying vascular remodeling. Expression levels of aldosterone and its receptor on tunica adventitia were determined using immunohistochemistry. Growth‑arrested AFs and tunica adventitia from rat vessels were incubated with UII and inhibitors of various signal transduction pathways. ALD receptor (ALD‑R) mRNA expression levels and ALD protein exoression levels were determined by reverse transcription‑quantitative polymerase chain reaction and ELISA, respectively. Aldosterone and its receptors were expressed on tunica adventitia. UII promoted ALD protein secretion from cells in a dose‑ and time‑dependent manner. ALD‑R mRNA expression in cells was also dysregulated. Furthermore, the effects of UII were substantially inhibited by treatment with the inhibitors PD98059, Y‑27632, H‑7, CSA and nicardipine. These results were further verified in the tunica adventitia of rat vessels. The present findings indicated that UII stimulated ALD protein secretion and ALD‑R mRNA expression in AFs and in the tunica adventitia of rat vessels; moreover, this effect may be mediated by signal transduction pathways involving MAPK, Rho, PKC, calcineurin and Ca2+. UII may also contribute to vascular remodeling by stimulating the production of ALD and its receptor. |
| doi_str_mv | 10.3892/mmr.2017.8233 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5783511</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1990445935</sourcerecordid><originalsourceid>FETCH-LOGICAL-c301t-66fbe29a881cab0754e0ce9911f13369ab2b3af9885ad39b2dd442471c6c04b63</originalsourceid><addsrcrecordid>eNpdkU1LxDAQhoMouq4evUrBi5eu-Wia5CKI-LEgCOKeQ5KmGmmbNUkX_fdmcV3U08wwDy8zPACcIDgjXOCLvg8zDBGbcUzIDpggJlBJIKx2Nz0Wgh2AwxjfIKwppmIfHGCBKcOMTcDTIvhkh-iGYj4vlsH3eYyF6hofkw1-sIX9WAYbo_NDkamgUqF8SM4UqlnZIbnkVFe0TgevOxVTPAJ7reqiPd7UKVjc3jxf35cPj3fz66uH0hCIUlnXrbZYKM6RURoyWllorBAItYiQWiiNNVGt4JyqhgiNm6aqcMWQqQ2sdE2m4PI7dznq3jYm3xJUJ5fB9Sp8Sq-c_LsZ3Kt88StJGScUoRxwvgkI_n20McneRWO7Tg3Wj1EiwThDHNYwo2f_0Dc_hiG_lykBq4oKQjNVflMm-BiDbbfHICjXtmS2Jde25NpW5k9_f7Clf_SQL_oIkkM</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1990445935</pqid></control><display><type>article</type><title>Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts</title><source>Spandidos Publications Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Li, Jun ; Zhang, Yong-Gang ; Luo, Li-Min ; Dong, Xiao ; Ding, Wen-Hui ; Dang, Shu-Yi</creator><creatorcontrib>Li, Jun ; Zhang, Yong-Gang ; Luo, Li-Min ; Dong, Xiao ; Ding, Wen-Hui ; Dang, Shu-Yi</creatorcontrib><description>Urotensin II (UII) contributes to cardiovascular diseases by activating vasoactive peptides. The present study aimed to determine the effect of UII on aldosterone (ALD) and its receptor in cultured adventitial fibroblasts (AFs) and the tunica adventitia of rat vessels to explore the possible mechanisms underlying vascular remodeling. Expression levels of aldosterone and its receptor on tunica adventitia were determined using immunohistochemistry. Growth‑arrested AFs and tunica adventitia from rat vessels were incubated with UII and inhibitors of various signal transduction pathways. ALD receptor (ALD‑R) mRNA expression levels and ALD protein exoression levels were determined by reverse transcription‑quantitative polymerase chain reaction and ELISA, respectively. Aldosterone and its receptors were expressed on tunica adventitia. UII promoted ALD protein secretion from cells in a dose‑ and time‑dependent manner. ALD‑R mRNA expression in cells was also dysregulated. Furthermore, the effects of UII were substantially inhibited by treatment with the inhibitors PD98059, Y‑27632, H‑7, CSA and nicardipine. These results were further verified in the tunica adventitia of rat vessels. The present findings indicated that UII stimulated ALD protein secretion and ALD‑R mRNA expression in AFs and in the tunica adventitia of rat vessels; moreover, this effect may be mediated by signal transduction pathways involving MAPK, Rho, PKC, calcineurin and Ca2+. UII may also contribute to vascular remodeling by stimulating the production of ALD and its receptor.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2017.8233</identifier><identifier>PMID: 29257277</identifier><language>eng</language><publisher>Greece: Spandidos Publications UK Ltd</publisher><subject>Aldosterone ; Aorta ; Atherosclerosis ; Calcineurin ; Calcium ; Cardiomyocytes ; Cardiovascular disease ; Cardiovascular diseases ; Cell adhesion & migration ; Coronary vessels ; Cytokines ; Diabetes ; Drug dosages ; Enzyme-linked immunosorbent assay ; Fibroblasts ; Gene expression ; Hypertension ; Hypotheses ; Immunoglobulins ; Immunohistochemistry ; Inflammation ; Kinases ; Laboratory animals ; MAP kinase ; Medical research ; Polymerase chain reaction ; Protein kinase C ; Proteins ; Reverse transcription ; Rodents ; Signal transduction ; Smooth muscle ; Vasoactive agents</subject><ispartof>Molecular medicine reports, 2018-02, Vol.17 (2), p.2921-2928</ispartof><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><rights>Copyright: © Li et al. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c301t-66fbe29a881cab0754e0ce9911f13369ab2b3af9885ad39b2dd442471c6c04b63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29257277$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Jun</creatorcontrib><creatorcontrib>Zhang, Yong-Gang</creatorcontrib><creatorcontrib>Luo, Li-Min</creatorcontrib><creatorcontrib>Dong, Xiao</creatorcontrib><creatorcontrib>Ding, Wen-Hui</creatorcontrib><creatorcontrib>Dang, Shu-Yi</creatorcontrib><title>Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Urotensin II (UII) contributes to cardiovascular diseases by activating vasoactive peptides. The present study aimed to determine the effect of UII on aldosterone (ALD) and its receptor in cultured adventitial fibroblasts (AFs) and the tunica adventitia of rat vessels to explore the possible mechanisms underlying vascular remodeling. Expression levels of aldosterone and its receptor on tunica adventitia were determined using immunohistochemistry. Growth‑arrested AFs and tunica adventitia from rat vessels were incubated with UII and inhibitors of various signal transduction pathways. ALD receptor (ALD‑R) mRNA expression levels and ALD protein exoression levels were determined by reverse transcription‑quantitative polymerase chain reaction and ELISA, respectively. Aldosterone and its receptors were expressed on tunica adventitia. UII promoted ALD protein secretion from cells in a dose‑ and time‑dependent manner. ALD‑R mRNA expression in cells was also dysregulated. Furthermore, the effects of UII were substantially inhibited by treatment with the inhibitors PD98059, Y‑27632, H‑7, CSA and nicardipine. These results were further verified in the tunica adventitia of rat vessels. The present findings indicated that UII stimulated ALD protein secretion and ALD‑R mRNA expression in AFs and in the tunica adventitia of rat vessels; moreover, this effect may be mediated by signal transduction pathways involving MAPK, Rho, PKC, calcineurin and Ca2+. UII may also contribute to vascular remodeling by stimulating the production of ALD and its receptor.</description><subject>Aldosterone</subject><subject>Aorta</subject><subject>Atherosclerosis</subject><subject>Calcineurin</subject><subject>Calcium</subject><subject>Cardiomyocytes</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Cell adhesion & migration</subject><subject>Coronary vessels</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Drug dosages</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Fibroblasts</subject><subject>Gene expression</subject><subject>Hypertension</subject><subject>Hypotheses</subject><subject>Immunoglobulins</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>MAP kinase</subject><subject>Medical research</subject><subject>Polymerase chain reaction</subject><subject>Protein kinase C</subject><subject>Proteins</subject><subject>Reverse transcription</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Smooth muscle</subject><subject>Vasoactive agents</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdkU1LxDAQhoMouq4evUrBi5eu-Wia5CKI-LEgCOKeQ5KmGmmbNUkX_fdmcV3U08wwDy8zPACcIDgjXOCLvg8zDBGbcUzIDpggJlBJIKx2Nz0Wgh2AwxjfIKwppmIfHGCBKcOMTcDTIvhkh-iGYj4vlsH3eYyF6hofkw1-sIX9WAYbo_NDkamgUqF8SM4UqlnZIbnkVFe0TgevOxVTPAJ7reqiPd7UKVjc3jxf35cPj3fz66uH0hCIUlnXrbZYKM6RURoyWllorBAItYiQWiiNNVGt4JyqhgiNm6aqcMWQqQ2sdE2m4PI7dznq3jYm3xJUJ5fB9Sp8Sq-c_LsZ3Kt88StJGScUoRxwvgkI_n20McneRWO7Tg3Wj1EiwThDHNYwo2f_0Dc_hiG_lykBq4oKQjNVflMm-BiDbbfHICjXtmS2Jde25NpW5k9_f7Clf_SQL_oIkkM</recordid><startdate>20180201</startdate><enddate>20180201</enddate><creator>Li, Jun</creator><creator>Zhang, Yong-Gang</creator><creator>Luo, Li-Min</creator><creator>Dong, Xiao</creator><creator>Ding, Wen-Hui</creator><creator>Dang, Shu-Yi</creator><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</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>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180201</creationdate><title>Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts</title><author>Li, Jun ; Zhang, Yong-Gang ; Luo, Li-Min ; Dong, Xiao ; Ding, Wen-Hui ; Dang, Shu-Yi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c301t-66fbe29a881cab0754e0ce9911f13369ab2b3af9885ad39b2dd442471c6c04b63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Aldosterone</topic><topic>Aorta</topic><topic>Atherosclerosis</topic><topic>Calcineurin</topic><topic>Calcium</topic><topic>Cardiomyocytes</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular diseases</topic><topic>Cell adhesion & migration</topic><topic>Coronary vessels</topic><topic>Cytokines</topic><topic>Diabetes</topic><topic>Drug dosages</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Fibroblasts</topic><topic>Gene expression</topic><topic>Hypertension</topic><topic>Hypotheses</topic><topic>Immunoglobulins</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>MAP kinase</topic><topic>Medical research</topic><topic>Polymerase chain reaction</topic><topic>Protein kinase C</topic><topic>Proteins</topic><topic>Reverse transcription</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Smooth muscle</topic><topic>Vasoactive agents</topic><toplevel>online_resources</toplevel><creatorcontrib>Li, Jun</creatorcontrib><creatorcontrib>Zhang, Yong-Gang</creatorcontrib><creatorcontrib>Luo, Li-Min</creatorcontrib><creatorcontrib>Dong, Xiao</creatorcontrib><creatorcontrib>Ding, Wen-Hui</creatorcontrib><creatorcontrib>Dang, Shu-Yi</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</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</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science 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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Jun</au><au>Zhang, Yong-Gang</au><au>Luo, Li-Min</au><au>Dong, Xiao</au><au>Ding, Wen-Hui</au><au>Dang, Shu-Yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2018-02-01</date><risdate>2018</risdate><volume>17</volume><issue>2</issue><spage>2921</spage><epage>2928</epage><pages>2921-2928</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Urotensin II (UII) contributes to cardiovascular diseases by activating vasoactive peptides. The present study aimed to determine the effect of UII on aldosterone (ALD) and its receptor in cultured adventitial fibroblasts (AFs) and the tunica adventitia of rat vessels to explore the possible mechanisms underlying vascular remodeling. Expression levels of aldosterone and its receptor on tunica adventitia were determined using immunohistochemistry. Growth‑arrested AFs and tunica adventitia from rat vessels were incubated with UII and inhibitors of various signal transduction pathways. ALD receptor (ALD‑R) mRNA expression levels and ALD protein exoression levels were determined by reverse transcription‑quantitative polymerase chain reaction and ELISA, respectively. Aldosterone and its receptors were expressed on tunica adventitia. UII promoted ALD protein secretion from cells in a dose‑ and time‑dependent manner. ALD‑R mRNA expression in cells was also dysregulated. Furthermore, the effects of UII were substantially inhibited by treatment with the inhibitors PD98059, Y‑27632, H‑7, CSA and nicardipine. These results were further verified in the tunica adventitia of rat vessels. The present findings indicated that UII stimulated ALD protein secretion and ALD‑R mRNA expression in AFs and in the tunica adventitia of rat vessels; moreover, this effect may be mediated by signal transduction pathways involving MAPK, Rho, PKC, calcineurin and Ca2+. UII may also contribute to vascular remodeling by stimulating the production of ALD and its receptor.</abstract><cop>Greece</cop><pub>Spandidos Publications UK Ltd</pub><pmid>29257277</pmid><doi>10.3892/mmr.2017.8233</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1791-2997 |
| ispartof | Molecular medicine reports, 2018-02, Vol.17 (2), p.2921-2928 |
| issn | 1791-2997 1791-3004 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5783511 |
| source | Spandidos Publications Journals; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Aldosterone Aorta Atherosclerosis Calcineurin Calcium Cardiomyocytes Cardiovascular disease Cardiovascular diseases Cell adhesion & migration Coronary vessels Cytokines Diabetes Drug dosages Enzyme-linked immunosorbent assay Fibroblasts Gene expression Hypertension Hypotheses Immunoglobulins Immunohistochemistry Inflammation Kinases Laboratory animals MAP kinase Medical research Polymerase chain reaction Protein kinase C Proteins Reverse transcription Rodents Signal transduction Smooth muscle Vasoactive agents |
| title | Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-09T12%3A09%3A58IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Urotensin%20II%20promotes%20aldosterone%20expression%20in%20rat%20aortic%20adventitial%20fibroblasts&rft.jtitle=Molecular%20medicine%20reports&rft.au=Li,%20Jun&rft.date=2018-02-01&rft.volume=17&rft.issue=2&rft.spage=2921&rft.epage=2928&rft.pages=2921-2928&rft.issn=1791-2997&rft.eissn=1791-3004&rft_id=info:doi/10.3892/mmr.2017.8233&rft_dat=%3Cproquest_pubme%3E1990445935%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1990445935&rft_id=info:pmid/29257277&rfr_iscdi=true |