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Influence of phenotype conversion of epicardial adipocytes on the coronary atherosclerosis and its potential molecular mechanism
To investigate the phenotype conversion of epicardial adipocytes and its potential molecular mechanism during the occurrence and development of coronary atherosclerosis. A total of 30 health male New Zealand white rabbits were used. In experiment group (n=15), rabbits were fed with high fat food to...
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Published in: | American journal of translational research 2015-01, Vol.7 (10), p.1712-1723 |
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creator | Wang, Jing Chen, Dong Cheng, Xun-Min Zhang, Qi-Gao Peng, Yong-Ping Wang, Li-Jun He, Song-Qing Gong, Jian-Bin |
description | To investigate the phenotype conversion of epicardial adipocytes and its potential molecular mechanism during the occurrence and development of coronary atherosclerosis.
A total of 30 health male New Zealand white rabbits were used. In experiment group (n=15), rabbits were fed with high fat food to establish atherosclerosis animal model; rabbits in control group (n=15) were fed with normal food.
At week 0, UCP-1 and PPARγ mRNA expressions in EAT and sBAT were significantly higher than in eWAT, and leptin mRNA expression lower than (P |
format | article |
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A total of 30 health male New Zealand white rabbits were used. In experiment group (n=15), rabbits were fed with high fat food to establish atherosclerosis animal model; rabbits in control group (n=15) were fed with normal food.
At week 0, UCP-1 and PPARγ mRNA expressions in EAT and sBAT were significantly higher than in eWAT, and leptin mRNA expression lower than (P<0.05). In experiment group, the mRNA expressions of UCP-1 and PPARγ reduced gradually, but leptin mRNA increased progressively in EAT (P<0.05). UCP-1 expression reduced gradually, the newly generated blood vessels reduced significantly, but leptin and RAM11 increased gradually (P<0.05). The adipocyte volume in EAT increased gradually, but the adipocyte number reduced progressively (P<0.05). The number of mitochondria with multiple crests reduced gradually in EAT; IL-6 reduced the mRNA expressions of UCP-1 and PPARγ in adipocytes of BAT in a dose dependent manner, but it increased the mRNA expressions of leptin and STAT3 (P<0.05). In the presence of IL-6, JSI-124 increased the mRNA expressions of UCP-1 and PPAR-γ in adipocytes of BAT in a dose dependent manner, but it reduced the mRNA expressions of leptin and STAT3 (P<0.05).
During the progression of atherosclerosis, there is a phenotype conversion of EAT from BAT to WAT, which further promotes the focal occurrence and development of atherosclerosis; IL-6 may activate JAK-STAT3 pathway to induce this conversion.]]></description><identifier>ISSN: 1943-8141</identifier><identifier>EISSN: 1943-8141</identifier><identifier>PMID: 26692919</identifier><language>eng</language><publisher>United States: e-Century Publishing Corporation</publisher><subject>Original</subject><ispartof>American journal of translational research, 2015-01, Vol.7 (10), p.1712-1723</ispartof><rights>AJTR Copyright © 2015 2015</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4656752/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4656752/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26692919$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Chen, Dong</creatorcontrib><creatorcontrib>Cheng, Xun-Min</creatorcontrib><creatorcontrib>Zhang, Qi-Gao</creatorcontrib><creatorcontrib>Peng, Yong-Ping</creatorcontrib><creatorcontrib>Wang, Li-Jun</creatorcontrib><creatorcontrib>He, Song-Qing</creatorcontrib><creatorcontrib>Gong, Jian-Bin</creatorcontrib><title>Influence of phenotype conversion of epicardial adipocytes on the coronary atherosclerosis and its potential molecular mechanism</title><title>American journal of translational research</title><addtitle>Am J Transl Res</addtitle><description><![CDATA[To investigate the phenotype conversion of epicardial adipocytes and its potential molecular mechanism during the occurrence and development of coronary atherosclerosis.
A total of 30 health male New Zealand white rabbits were used. In experiment group (n=15), rabbits were fed with high fat food to establish atherosclerosis animal model; rabbits in control group (n=15) were fed with normal food.
At week 0, UCP-1 and PPARγ mRNA expressions in EAT and sBAT were significantly higher than in eWAT, and leptin mRNA expression lower than (P<0.05). In experiment group, the mRNA expressions of UCP-1 and PPARγ reduced gradually, but leptin mRNA increased progressively in EAT (P<0.05). UCP-1 expression reduced gradually, the newly generated blood vessels reduced significantly, but leptin and RAM11 increased gradually (P<0.05). The adipocyte volume in EAT increased gradually, but the adipocyte number reduced progressively (P<0.05). The number of mitochondria with multiple crests reduced gradually in EAT; IL-6 reduced the mRNA expressions of UCP-1 and PPARγ in adipocytes of BAT in a dose dependent manner, but it increased the mRNA expressions of leptin and STAT3 (P<0.05). In the presence of IL-6, JSI-124 increased the mRNA expressions of UCP-1 and PPAR-γ in adipocytes of BAT in a dose dependent manner, but it reduced the mRNA expressions of leptin and STAT3 (P<0.05).
During the progression of atherosclerosis, there is a phenotype conversion of EAT from BAT to WAT, which further promotes the focal occurrence and development of atherosclerosis; IL-6 may activate JAK-STAT3 pathway to induce this conversion.]]></description><subject>Original</subject><issn>1943-8141</issn><issn>1943-8141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNpVUE1LxDAQLaK46-pfkBy9FJo2TZuLIIsfC4IXPZd0OnUjaRKTdGFv_nRbXGWdw3y-efOYk2RJBSvSmjJ6epQvkosQPrKMl4Ln58ki51zkgopl8rUxvR7RABLbE7dFY-PeIQFrduiDsmbuo1MgfaekJrJTzsI-YiDTLG5nqLdG-j2RU-VtAD17FYg0HVExEGcjmjgvD1YjjFp6MiBspVFhuEzOeqkDXh3iKnl7uH9dP6XPL4-b9d1z6iaxMW2BipoLgYBZ1ldssr4ARkvASmalANp2KCrgkNVYM2irDAALxgDrvJB5sUpuf3jd2A7YwaTIS904r4ZJe2Olav5PjNo273bXMF7yqpwJbg4E3n6OGGIzqACotTRox9DQqqSsFkyICXp9fOvvyO_bi2-7cIUe</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Wang, Jing</creator><creator>Chen, Dong</creator><creator>Cheng, Xun-Min</creator><creator>Zhang, Qi-Gao</creator><creator>Peng, Yong-Ping</creator><creator>Wang, Li-Jun</creator><creator>He, Song-Qing</creator><creator>Gong, Jian-Bin</creator><general>e-Century Publishing Corporation</general><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150101</creationdate><title>Influence of phenotype conversion of epicardial adipocytes on the coronary atherosclerosis and its potential molecular mechanism</title><author>Wang, Jing ; Chen, Dong ; Cheng, Xun-Min ; Zhang, Qi-Gao ; Peng, Yong-Ping ; Wang, Li-Jun ; He, Song-Qing ; Gong, Jian-Bin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p266t-bc198699ece00f74444f3c415ce7a059c1bde97c6c08e84cb70cce344ce823a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Original</topic><toplevel>online_resources</toplevel><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Chen, Dong</creatorcontrib><creatorcontrib>Cheng, Xun-Min</creatorcontrib><creatorcontrib>Zhang, Qi-Gao</creatorcontrib><creatorcontrib>Peng, Yong-Ping</creatorcontrib><creatorcontrib>Wang, Li-Jun</creatorcontrib><creatorcontrib>He, Song-Qing</creatorcontrib><creatorcontrib>Gong, Jian-Bin</creatorcontrib><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of translational research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Jing</au><au>Chen, Dong</au><au>Cheng, Xun-Min</au><au>Zhang, Qi-Gao</au><au>Peng, Yong-Ping</au><au>Wang, Li-Jun</au><au>He, Song-Qing</au><au>Gong, Jian-Bin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Influence of phenotype conversion of epicardial adipocytes on the coronary atherosclerosis and its potential molecular mechanism</atitle><jtitle>American journal of translational research</jtitle><addtitle>Am J Transl Res</addtitle><date>2015-01-01</date><risdate>2015</risdate><volume>7</volume><issue>10</issue><spage>1712</spage><epage>1723</epage><pages>1712-1723</pages><issn>1943-8141</issn><eissn>1943-8141</eissn><abstract><![CDATA[To investigate the phenotype conversion of epicardial adipocytes and its potential molecular mechanism during the occurrence and development of coronary atherosclerosis.
A total of 30 health male New Zealand white rabbits were used. In experiment group (n=15), rabbits were fed with high fat food to establish atherosclerosis animal model; rabbits in control group (n=15) were fed with normal food.
At week 0, UCP-1 and PPARγ mRNA expressions in EAT and sBAT were significantly higher than in eWAT, and leptin mRNA expression lower than (P<0.05). In experiment group, the mRNA expressions of UCP-1 and PPARγ reduced gradually, but leptin mRNA increased progressively in EAT (P<0.05). UCP-1 expression reduced gradually, the newly generated blood vessels reduced significantly, but leptin and RAM11 increased gradually (P<0.05). The adipocyte volume in EAT increased gradually, but the adipocyte number reduced progressively (P<0.05). The number of mitochondria with multiple crests reduced gradually in EAT; IL-6 reduced the mRNA expressions of UCP-1 and PPARγ in adipocytes of BAT in a dose dependent manner, but it increased the mRNA expressions of leptin and STAT3 (P<0.05). In the presence of IL-6, JSI-124 increased the mRNA expressions of UCP-1 and PPAR-γ in adipocytes of BAT in a dose dependent manner, but it reduced the mRNA expressions of leptin and STAT3 (P<0.05).
During the progression of atherosclerosis, there is a phenotype conversion of EAT from BAT to WAT, which further promotes the focal occurrence and development of atherosclerosis; IL-6 may activate JAK-STAT3 pathway to induce this conversion.]]></abstract><cop>United States</cop><pub>e-Century Publishing Corporation</pub><pmid>26692919</pmid><tpages>12</tpages></addata></record> |
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title | Influence of phenotype conversion of epicardial adipocytes on the coronary atherosclerosis and its potential molecular mechanism |
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