Thymic stromal lymphopoietin-induced HOTAIR activation promotes endothelial cell proliferation and migration in atherosclerosis
Endothelial cells' (EC) injury is a major step for the pathological progression of atherosclerosis. Recent study demonstrated that thymic stromal lymphopoietin (TSLP) exerts a protective role in atherosclerosis. However, the effect of TSLP and the exact molecular mechanism involved in EC remain...
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| Veröffentlicht in: | Bioscience reports 2017-08, Vol.37 (4) |
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| creator | Peng, Yudong Meng, Kai Jiang, Lili Zhong, Yucheng Yang, Yong Lan, Yin Zeng, Qiutang Cheng, Longxian |
| description | Endothelial cells' (EC) injury is a major step for the pathological progression of atherosclerosis. Recent study demonstrated that thymic stromal lymphopoietin (TSLP) exerts a protective role in atherosclerosis. However, the effect of TSLP and the exact molecular mechanism involved in EC remains unknown. In the present study, we found that long noncoding RNA (lncRNA) HOTAIR was much lower in EC from atherosclerotic plaque. Functional assays showed that HOTAIR facilitated cell proliferation and migration, and suppressed apoptosis in EC. Moreover, we demonstrated that TSLP functions upstream of HOTAIR. We found that serum level of TSLP was decreased in atherosclerosis patients and serum TSLP level positively correlated with HOTAIR expression in EC. Further investigation demonstrated that TSLP activated HOTAIR transcription through PI3K/AKT-IRF1 pathway and then regulates the EC proliferation and migration. TSLP-HOTAIR axis also plays a protective role in low-density lipoprotein (ox-LDL)-induced EC injury. Taken together, TSLP-HOTAIR may be a potential therapy for EC dysfunction in atherosclerosis. |
| doi_str_mv | 10.1042/BSR20170351 |
| format | Article |
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Recent study demonstrated that thymic stromal lymphopoietin (TSLP) exerts a protective role in atherosclerosis. However, the effect of TSLP and the exact molecular mechanism involved in EC remains unknown. In the present study, we found that long noncoding RNA (lncRNA) HOTAIR was much lower in EC from atherosclerotic plaque. Functional assays showed that HOTAIR facilitated cell proliferation and migration, and suppressed apoptosis in EC. Moreover, we demonstrated that TSLP functions upstream of HOTAIR. We found that serum level of TSLP was decreased in atherosclerosis patients and serum TSLP level positively correlated with HOTAIR expression in EC. Further investigation demonstrated that TSLP activated HOTAIR transcription through PI3K/AKT-IRF1 pathway and then regulates the EC proliferation and migration. TSLP-HOTAIR axis also plays a protective role in low-density lipoprotein (ox-LDL)-induced EC injury. Taken together, TSLP-HOTAIR may be a potential therapy for EC dysfunction in atherosclerosis.</description><identifier>ISSN: 0144-8463</identifier><identifier>EISSN: 1573-4935</identifier><identifier>DOI: 10.1042/BSR20170351</identifier><identifier>PMID: 28615347</identifier><language>eng</language><publisher>England: Portland Press Ltd</publisher><subject>Atherosclerosis - metabolism ; Atherosclerosis - pathology ; Cell Line ; Cell Movement ; Cell Proliferation ; Cytokines - metabolism ; Human Umbilical Vein Endothelial Cells ; Humans ; Interferon Regulatory Factor-1 - metabolism ; Lipoproteins, LDL - pharmacology ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; RNA, Long Noncoding - biosynthesis</subject><ispartof>Bioscience reports, 2017-08, Vol.37 (4)</ispartof><rights>2017 The Author(s).</rights><rights>2017 The Author(s). 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-bf4bff48ae5190c166e34120f523ddfa42ec0d9759c637ac9e477ef09300d2ad3</citedby><cites>FETCH-LOGICAL-c447t-bf4bff48ae5190c166e34120f523ddfa42ec0d9759c637ac9e477ef09300d2ad3</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/PMC5518535/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5518535/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28615347$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Peng, Yudong</creatorcontrib><creatorcontrib>Meng, Kai</creatorcontrib><creatorcontrib>Jiang, Lili</creatorcontrib><creatorcontrib>Zhong, Yucheng</creatorcontrib><creatorcontrib>Yang, Yong</creatorcontrib><creatorcontrib>Lan, Yin</creatorcontrib><creatorcontrib>Zeng, Qiutang</creatorcontrib><creatorcontrib>Cheng, Longxian</creatorcontrib><title>Thymic stromal lymphopoietin-induced HOTAIR activation promotes endothelial cell proliferation and migration in atherosclerosis</title><title>Bioscience reports</title><addtitle>Biosci Rep</addtitle><description>Endothelial cells' (EC) injury is a major step for the pathological progression of atherosclerosis. Recent study demonstrated that thymic stromal lymphopoietin (TSLP) exerts a protective role in atherosclerosis. However, the effect of TSLP and the exact molecular mechanism involved in EC remains unknown. In the present study, we found that long noncoding RNA (lncRNA) HOTAIR was much lower in EC from atherosclerotic plaque. Functional assays showed that HOTAIR facilitated cell proliferation and migration, and suppressed apoptosis in EC. Moreover, we demonstrated that TSLP functions upstream of HOTAIR. We found that serum level of TSLP was decreased in atherosclerosis patients and serum TSLP level positively correlated with HOTAIR expression in EC. Further investigation demonstrated that TSLP activated HOTAIR transcription through PI3K/AKT-IRF1 pathway and then regulates the EC proliferation and migration. TSLP-HOTAIR axis also plays a protective role in low-density lipoprotein (ox-LDL)-induced EC injury. Taken together, TSLP-HOTAIR may be a potential therapy for EC dysfunction in atherosclerosis.</description><subject>Atherosclerosis - metabolism</subject><subject>Atherosclerosis - pathology</subject><subject>Cell Line</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cytokines - metabolism</subject><subject>Human Umbilical Vein Endothelial Cells</subject><subject>Humans</subject><subject>Interferon Regulatory Factor-1 - metabolism</subject><subject>Lipoproteins, LDL - pharmacology</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>RNA, Long Noncoding - biosynthesis</subject><issn>0144-8463</issn><issn>1573-4935</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc1LxDAQxYMoun6cvEuPglSTJmnai6DiFwiCrueQTSZuJG1qk13Yk_-6LbuKXjIk7zdvMjyEjgk-J5gVF9evLwUmAlNOttCEcEFzVlO-jSaYMJZXrKR7aD_GD4zxILBdtFdUJeGUiQn6ms5XjdNZTH1olM_8qunmoQsOkmtz15qFBpM9PE-vHl8ypZNbquRCm3UDHhLEDFoT0hy8G5o1eD8q3lno15xqTda4983NDQ8D3Ieo_Xi6eIh2rPIRjjb1AL3d3U5vHvKn5_vHm6unXDMmUj6zbGYtqxRwUmNNyhIoIwW2vKDGWMUK0NjUgte6pELpGpgQYHFNMTaFMvQAXa59u8WsAaOhTb3ysutdo_qVDMrJ_0rr5vI9LCXnpOKUDwanG4M-fC4gJtm4OC6sWgiLKElNMKWCVSN6tkb1sGLswf6OIViOkck_kQ30yd-f_bI_GdFvseeWFQ</recordid><startdate>20170831</startdate><enddate>20170831</enddate><creator>Peng, Yudong</creator><creator>Meng, Kai</creator><creator>Jiang, Lili</creator><creator>Zhong, Yucheng</creator><creator>Yang, Yong</creator><creator>Lan, Yin</creator><creator>Zeng, Qiutang</creator><creator>Cheng, Longxian</creator><general>Portland Press Ltd</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170831</creationdate><title>Thymic stromal lymphopoietin-induced HOTAIR activation promotes endothelial cell proliferation and migration in atherosclerosis</title><author>Peng, Yudong ; Meng, Kai ; Jiang, Lili ; Zhong, Yucheng ; Yang, Yong ; Lan, Yin ; Zeng, Qiutang ; Cheng, Longxian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-bf4bff48ae5190c166e34120f523ddfa42ec0d9759c637ac9e477ef09300d2ad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Atherosclerosis - metabolism</topic><topic>Atherosclerosis - pathology</topic><topic>Cell Line</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cytokines - metabolism</topic><topic>Human Umbilical Vein Endothelial Cells</topic><topic>Humans</topic><topic>Interferon Regulatory Factor-1 - metabolism</topic><topic>Lipoproteins, LDL - pharmacology</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>RNA, Long Noncoding - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Peng, Yudong</creatorcontrib><creatorcontrib>Meng, Kai</creatorcontrib><creatorcontrib>Jiang, Lili</creatorcontrib><creatorcontrib>Zhong, Yucheng</creatorcontrib><creatorcontrib>Yang, Yong</creatorcontrib><creatorcontrib>Lan, Yin</creatorcontrib><creatorcontrib>Zeng, Qiutang</creatorcontrib><creatorcontrib>Cheng, Longxian</creatorcontrib><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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Bioscience reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Peng, Yudong</au><au>Meng, Kai</au><au>Jiang, Lili</au><au>Zhong, Yucheng</au><au>Yang, Yong</au><au>Lan, Yin</au><au>Zeng, Qiutang</au><au>Cheng, Longxian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thymic stromal lymphopoietin-induced HOTAIR activation promotes endothelial cell proliferation and migration in atherosclerosis</atitle><jtitle>Bioscience reports</jtitle><addtitle>Biosci Rep</addtitle><date>2017-08-31</date><risdate>2017</risdate><volume>37</volume><issue>4</issue><issn>0144-8463</issn><eissn>1573-4935</eissn><abstract>Endothelial cells' (EC) injury is a major step for the pathological progression of atherosclerosis. Recent study demonstrated that thymic stromal lymphopoietin (TSLP) exerts a protective role in atherosclerosis. However, the effect of TSLP and the exact molecular mechanism involved in EC remains unknown. In the present study, we found that long noncoding RNA (lncRNA) HOTAIR was much lower in EC from atherosclerotic plaque. Functional assays showed that HOTAIR facilitated cell proliferation and migration, and suppressed apoptosis in EC. Moreover, we demonstrated that TSLP functions upstream of HOTAIR. We found that serum level of TSLP was decreased in atherosclerosis patients and serum TSLP level positively correlated with HOTAIR expression in EC. Further investigation demonstrated that TSLP activated HOTAIR transcription through PI3K/AKT-IRF1 pathway and then regulates the EC proliferation and migration. TSLP-HOTAIR axis also plays a protective role in low-density lipoprotein (ox-LDL)-induced EC injury. Taken together, TSLP-HOTAIR may be a potential therapy for EC dysfunction in atherosclerosis.</abstract><cop>England</cop><pub>Portland Press Ltd</pub><pmid>28615347</pmid><doi>10.1042/BSR20170351</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Atherosclerosis - metabolism Atherosclerosis - pathology Cell Line Cell Movement Cell Proliferation Cytokines - metabolism Human Umbilical Vein Endothelial Cells Humans Interferon Regulatory Factor-1 - metabolism Lipoproteins, LDL - pharmacology Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism RNA, Long Noncoding - biosynthesis |
| title | Thymic stromal lymphopoietin-induced HOTAIR activation promotes endothelial cell proliferation and migration in atherosclerosis |
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