Resistin increases monolayer permeability of human coronary artery endothelial cells
Resistin has been linked to obesity, insulin resistance, atherosclerosis, and the development of cardiovascular disease. Nevertheless, the effects and the molecular mechanisms of resistin on endothelial permeability, a key event in the development of atherosclerosis, inflammation, and vascular disea...
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| description | Resistin has been linked to obesity, insulin resistance, atherosclerosis, and the development of cardiovascular disease. Nevertheless, the effects and the molecular mechanisms of resistin on endothelial permeability, a key event in the development of atherosclerosis, inflammation, and vascular disease, are largely unknown. In order to determine the effect of resistin on endothelial permeability, human coronary artery endothelial cells (HCAECs) were treated with clinically relevant concentrations of resistin and the endothelial permeability was measured using the Transwell system with a Texas-Red-labeled dextran tracer. The permeability of HCAEC monolayers treated with resistin (80 ng/mL) was 51% higher than the permeability of control monolayers (P |
| doi_str_mv | 10.1371/journal.pone.0084576 |
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Nevertheless, the effects and the molecular mechanisms of resistin on endothelial permeability, a key event in the development of atherosclerosis, inflammation, and vascular disease, are largely unknown. In order to determine the effect of resistin on endothelial permeability, human coronary artery endothelial cells (HCAECs) were treated with clinically relevant concentrations of resistin and the endothelial permeability was measured using the Transwell system with a Texas-Red-labeled dextran tracer. The permeability of HCAEC monolayers treated with resistin (80 ng/mL) was 51% higher than the permeability of control monolayers (P<0.05). The mRNA levels of tight junction proteins zonula occludens-1 (ZO-1) and occludin in resistin-treated cells were 37% and 42% lower, respectively, than the corresponding levels in untreated cells. The protein levels of these molecules in resistin-treated cells were significantly reduced by 35% and 37%, respectively (P<0.05), as shown by flow cytometry and Western blot analysis. Superoxide dismutase (SOD) mimetic MnTBAP effectively blocked the resistin-mediated reduction of ZO-1 and occludin levels in HCAECs. In addition, superoxide anion production was increased from 21% (untreated cells) to 55% (cells treated with 40 ng/mL resistin), and 64% (resistin, 80 mg/mL) (P<0.05). The natural antioxidant Ginkgolide A effectively inhibited resistin-induced increase in permeability and the increase in superoxide anion production in HCAECs. Furthermore, resistin treatment significantly activated p38 MAPK, but not ERK1/2. Pretreatment of HCAECs with a p38 inhibitor effectively blocked resistin-induced permeability. These results provide new evidence that resistin may contribute to the vascular lesion formation via increasing endothelial permeability through the mechanism of oxidative stress and the activation of p38 MAPK.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0084576</identifier><identifier>PMID: 24386395</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Anions ; Antioxidants ; Arteriosclerosis ; Atherosclerosis ; Biology ; Capillary Permeability ; Cardiovascular disease ; Cardiovascular diseases ; Cells, Cultured ; Chemistry ; Coronary artery ; Coronary vessels ; Coronary Vessels - cytology ; Coronary Vessels - metabolism ; Cytometry ; Dextran ; Dextrans ; Endothelial cells ; Endothelial Cells - cytology ; Endothelial Cells - metabolism ; Endothelium ; Enzyme Activation ; Extracellular signal-regulated kinase ; Flow cytometry ; Growth factors ; Humans ; Immunoglobulins ; Inflammation ; Insulin ; Insulin resistance ; Kinases ; Laboratories ; MAP kinase ; MAP Kinase Signaling System ; Medicine ; Membrane permeability ; Molecular modelling ; Monolayers ; Monomolecular films ; mRNA ; Obesity ; Oxidative Stress ; p38 Mitogen-Activated Protein Kinases - metabolism ; Permeability ; Phosphorylation ; Pretreatment ; Proteins ; Resistin - metabolism ; RNA ; RNA, Messenger - metabolism ; Rodents ; Signal transduction ; Superoxide dismutase ; Superoxide Dismutase - metabolism ; Superoxides ; Surgeons ; Surgery ; Tracers (Biology) ; Tumor necrosis factor-TNF ; Vascular diseases ; Zonula occludens-1 protein ; Zonula Occludens-1 Protein - metabolism</subject><ispartof>PloS one, 2013-12, Vol.8 (12), p.e84576-e84576</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Jamaluddin et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Jamaluddin et al 2013 Jamaluddin et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-3eb96de35127d9e8ffca75f52e7e7ef39df3975a8f177a6b2e0d0f05a09771cd3</citedby><cites>FETCH-LOGICAL-c692t-3eb96de35127d9e8ffca75f52e7e7ef39df3975a8f177a6b2e0d0f05a09771cd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3874001/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3874001/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24386395$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jamaluddin, Md Saha</creatorcontrib><creatorcontrib>Yan, Shaoyu</creatorcontrib><creatorcontrib>Lü, Jianming</creatorcontrib><creatorcontrib>Liang, Zhengdong</creatorcontrib><creatorcontrib>Yao, Qizhi</creatorcontrib><creatorcontrib>Chen, Changyi</creatorcontrib><title>Resistin increases monolayer permeability of human coronary artery endothelial cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Resistin has been linked to obesity, insulin resistance, atherosclerosis, and the development of cardiovascular disease. Nevertheless, the effects and the molecular mechanisms of resistin on endothelial permeability, a key event in the development of atherosclerosis, inflammation, and vascular disease, are largely unknown. In order to determine the effect of resistin on endothelial permeability, human coronary artery endothelial cells (HCAECs) were treated with clinically relevant concentrations of resistin and the endothelial permeability was measured using the Transwell system with a Texas-Red-labeled dextran tracer. The permeability of HCAEC monolayers treated with resistin (80 ng/mL) was 51% higher than the permeability of control monolayers (P<0.05). The mRNA levels of tight junction proteins zonula occludens-1 (ZO-1) and occludin in resistin-treated cells were 37% and 42% lower, respectively, than the corresponding levels in untreated cells. The protein levels of these molecules in resistin-treated cells were significantly reduced by 35% and 37%, respectively (P<0.05), as shown by flow cytometry and Western blot analysis. Superoxide dismutase (SOD) mimetic MnTBAP effectively blocked the resistin-mediated reduction of ZO-1 and occludin levels in HCAECs. In addition, superoxide anion production was increased from 21% (untreated cells) to 55% (cells treated with 40 ng/mL resistin), and 64% (resistin, 80 mg/mL) (P<0.05). The natural antioxidant Ginkgolide A effectively inhibited resistin-induced increase in permeability and the increase in superoxide anion production in HCAECs. Furthermore, resistin treatment significantly activated p38 MAPK, but not ERK1/2. Pretreatment of HCAECs with a p38 inhibitor effectively blocked resistin-induced permeability. These results provide new evidence that resistin may contribute to the vascular lesion formation via increasing endothelial permeability through the mechanism of oxidative stress and the activation of p38 MAPK.</description><subject>Analysis</subject><subject>Anions</subject><subject>Antioxidants</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Biology</subject><subject>Capillary Permeability</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Cells, Cultured</subject><subject>Chemistry</subject><subject>Coronary artery</subject><subject>Coronary vessels</subject><subject>Coronary Vessels - cytology</subject><subject>Coronary Vessels - metabolism</subject><subject>Cytometry</subject><subject>Dextran</subject><subject>Dextrans</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - cytology</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelium</subject><subject>Enzyme Activation</subject><subject>Extracellular signal-regulated kinase</subject><subject>Flow cytometry</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Immunoglobulins</subject><subject>Inflammation</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>MAP kinase</subject><subject>MAP Kinase Signaling System</subject><subject>Medicine</subject><subject>Membrane permeability</subject><subject>Molecular modelling</subject><subject>Monolayers</subject><subject>Monomolecular films</subject><subject>mRNA</subject><subject>Obesity</subject><subject>Oxidative Stress</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Permeability</subject><subject>Phosphorylation</subject><subject>Pretreatment</subject><subject>Proteins</subject><subject>Resistin - metabolism</subject><subject>RNA</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Superoxides</subject><subject>Surgeons</subject><subject>Surgery</subject><subject>Tracers (Biology)</subject><subject>Tumor necrosis factor-TNF</subject><subject>Vascular diseases</subject><subject>Zonula occludens-1 protein</subject><subject>Zonula Occludens-1 Protein - metabolism</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl1rFDEUhgdRbK3-A9EBQfRi13zMJJMboRQ_FgqFWr0N2cnJbkomWZMZcf-9GXdadqQXEkIOyXPe5Jy8RfESoyWmHH-4DUP0yi13wcMSoaaqOXtUnGJByYIRRB8fxSfFs5RuEappw9jT4oRUOaCiPi1uriHZ1FtfWt9GUAlS2QUfnNpDLHcQO1Br62y_L4Mpt0OnfNmGGLyK-1LFHvICXod-C84qV7bgXHpePDHKJXgxrWfF98-fbi6-Li6vvqwuzi8XLROkX1BYC6aB1phwLaAxplW8NjUBnoehQufJa9UYzLliawJII4NqhQTnuNX0rHh90N25kOTUkCRxxTGqaiF4JlYHQgd1K3fRdvndMigr_26EuJG5CNs6kFpTTIhZM41ZxdRaKMU1bahhiFBK66z1cbptWHegW_B9VG4mOj_xdis34ZekDa8Qwlng3SQQw88BUi87m8aGKQ9hGN8tEEc1oyP65h_04eomaqNyAdabkO9tR1F5XnEuGkJJk6nlA1QeGjrbZvcYm_dnCe9nCZnp4Xe_UUNKcvXt-v_Zqx9z9u0RuwXl-m0Kbuht8GkOVgewjSGlCOa-yRjJ0fx33ZCj-eVk_pz26viD7pPu3E7_AKbtAFo</recordid><startdate>20131227</startdate><enddate>20131227</enddate><creator>Jamaluddin, Md Saha</creator><creator>Yan, Shaoyu</creator><creator>Lü, Jianming</creator><creator>Liang, Zhengdong</creator><creator>Yao, Qizhi</creator><creator>Chen, Changyi</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20131227</creationdate><title>Resistin increases monolayer permeability of human coronary artery endothelial cells</title><author>Jamaluddin, Md Saha ; Yan, Shaoyu ; Lü, Jianming ; Liang, Zhengdong ; Yao, Qizhi ; Chen, Changyi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-3eb96de35127d9e8ffca75f52e7e7ef39df3975a8f177a6b2e0d0f05a09771cd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Analysis</topic><topic>Anions</topic><topic>Antioxidants</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Biology</topic><topic>Capillary Permeability</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular diseases</topic><topic>Cells, Cultured</topic><topic>Chemistry</topic><topic>Coronary artery</topic><topic>Coronary vessels</topic><topic>Coronary Vessels - cytology</topic><topic>Coronary Vessels - metabolism</topic><topic>Cytometry</topic><topic>Dextran</topic><topic>Dextrans</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - cytology</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelium</topic><topic>Enzyme Activation</topic><topic>Extracellular signal-regulated kinase</topic><topic>Flow cytometry</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Immunoglobulins</topic><topic>Inflammation</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>MAP kinase</topic><topic>MAP Kinase Signaling System</topic><topic>Medicine</topic><topic>Membrane permeability</topic><topic>Molecular modelling</topic><topic>Monolayers</topic><topic>Monomolecular films</topic><topic>mRNA</topic><topic>Obesity</topic><topic>Oxidative Stress</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Permeability</topic><topic>Phosphorylation</topic><topic>Pretreatment</topic><topic>Proteins</topic><topic>Resistin - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jamaluddin, Md Saha</au><au>Yan, Shaoyu</au><au>Lü, Jianming</au><au>Liang, Zhengdong</au><au>Yao, Qizhi</au><au>Chen, Changyi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Resistin increases monolayer permeability of human coronary artery endothelial cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-12-27</date><risdate>2013</risdate><volume>8</volume><issue>12</issue><spage>e84576</spage><epage>e84576</epage><pages>e84576-e84576</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Resistin has been linked to obesity, insulin resistance, atherosclerosis, and the development of cardiovascular disease. Nevertheless, the effects and the molecular mechanisms of resistin on endothelial permeability, a key event in the development of atherosclerosis, inflammation, and vascular disease, are largely unknown. In order to determine the effect of resistin on endothelial permeability, human coronary artery endothelial cells (HCAECs) were treated with clinically relevant concentrations of resistin and the endothelial permeability was measured using the Transwell system with a Texas-Red-labeled dextran tracer. The permeability of HCAEC monolayers treated with resistin (80 ng/mL) was 51% higher than the permeability of control monolayers (P<0.05). The mRNA levels of tight junction proteins zonula occludens-1 (ZO-1) and occludin in resistin-treated cells were 37% and 42% lower, respectively, than the corresponding levels in untreated cells. The protein levels of these molecules in resistin-treated cells were significantly reduced by 35% and 37%, respectively (P<0.05), as shown by flow cytometry and Western blot analysis. Superoxide dismutase (SOD) mimetic MnTBAP effectively blocked the resistin-mediated reduction of ZO-1 and occludin levels in HCAECs. In addition, superoxide anion production was increased from 21% (untreated cells) to 55% (cells treated with 40 ng/mL resistin), and 64% (resistin, 80 mg/mL) (P<0.05). The natural antioxidant Ginkgolide A effectively inhibited resistin-induced increase in permeability and the increase in superoxide anion production in HCAECs. Furthermore, resistin treatment significantly activated p38 MAPK, but not ERK1/2. Pretreatment of HCAECs with a p38 inhibitor effectively blocked resistin-induced permeability. These results provide new evidence that resistin may contribute to the vascular lesion formation via increasing endothelial permeability through the mechanism of oxidative stress and the activation of p38 MAPK.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24386395</pmid><doi>10.1371/journal.pone.0084576</doi><tpages>e84576</tpages><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1471045997 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Analysis Anions Antioxidants Arteriosclerosis Atherosclerosis Biology Capillary Permeability Cardiovascular disease Cardiovascular diseases Cells, Cultured Chemistry Coronary artery Coronary vessels Coronary Vessels - cytology Coronary Vessels - metabolism Cytometry Dextran Dextrans Endothelial cells Endothelial Cells - cytology Endothelial Cells - metabolism Endothelium Enzyme Activation Extracellular signal-regulated kinase Flow cytometry Growth factors Humans Immunoglobulins Inflammation Insulin Insulin resistance Kinases Laboratories MAP kinase MAP Kinase Signaling System Medicine Membrane permeability Molecular modelling Monolayers Monomolecular films mRNA Obesity Oxidative Stress p38 Mitogen-Activated Protein Kinases - metabolism Permeability Phosphorylation Pretreatment Proteins Resistin - metabolism RNA RNA, Messenger - metabolism Rodents Signal transduction Superoxide dismutase Superoxide Dismutase - metabolism Superoxides Surgeons Surgery Tracers (Biology) Tumor necrosis factor-TNF Vascular diseases Zonula occludens-1 protein Zonula Occludens-1 Protein - metabolism |
| title | Resistin increases monolayer permeability of human coronary artery endothelial cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-21T18%3A41%3A31IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Resistin%20increases%20monolayer%20permeability%20of%20human%20coronary%20artery%20endothelial%20cells&rft.jtitle=PloS%20one&rft.au=Jamaluddin,%20Md%20Saha&rft.date=2013-12-27&rft.volume=8&rft.issue=12&rft.spage=e84576&rft.epage=e84576&rft.pages=e84576-e84576&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0084576&rft_dat=%3Cgale_plos_%3EA477982328%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1471045997&rft_id=info:pmid/24386395&rft_galeid=A477982328&rft_doaj_id=oai_doaj_org_article_dd3122fb6d1646ab9aa7d383f6023335&rfr_iscdi=true |