Long noncoding RNA p21 enhances autophagy to alleviate endothelial progenitor cells damage and promote endothelial repair in hypertension through SESN2/AMPK/TSC2 pathway
Vascular damage of hypertension has been the focus of hypertension treatment, and endothelial progenitor cells (EPCs) play an important role in the repair of vascular endothelial damage. Functional damage and decreased number of EPCs are observed in the peripheral circulation of hypertensive patient...
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| Veröffentlicht in: | Pharmacological research 2021-11, Vol.173, p.105920-105920, Article 105920 |
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| creator | Li, Chao Lin, Lin Zhang, Lei Xu, Ran Chen, Xiaoqing Ji, Jingkang Li, Yunlun |
| description | Vascular damage of hypertension has been the focus of hypertension treatment, and endothelial progenitor cells (EPCs) play an important role in the repair of vascular endothelial damage. Functional damage and decreased number of EPCs are observed in the peripheral circulation of hypertensive patients, but its mechanism is not yet elucidated. Here, we show that the number of EPCs in hypertensive patients is significantly lower than that of normal population, and the cell function decreases with a higher proportion of EPCs at later stages. A decrease in autophagy is responsible for the senescence and damage of EPCs induced by AngII. Moreover, lncRNA-p21 plays a critical regulator role in EPCs’ senescence and dysfunction. Furthermore, lncRNA-p21 activates SESN2/AMPK/TSC2 pathway by promoting the transcriptional activity of p53 and enhances autophagy to protect against AngII-induced EPC damage. The data provide evidence that a reversal of decreased autophagy serves as the protective mechanism of EPC injury in hypertensive patients, and lncRNA-p21 is a new therapeutic target for vascular endothelial repair in hypertension.
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| doi_str_mv | 10.1016/j.phrs.2021.105920 |
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[Display omitted]</description><identifier>ISSN: 1043-6618</identifier><identifier>EISSN: 1096-1186</identifier><identifier>DOI: 10.1016/j.phrs.2021.105920</identifier><identifier>PMID: 34601081</identifier><language>eng</language><publisher>Netherlands: Elsevier Ltd</publisher><subject>Aged ; AMP-Activated Protein Kinases - metabolism ; Angiotensin II ; Animals ; Autophagy ; beta-Galactosidase - metabolism ; Cell Adhesion ; Cell Movement ; Endothelial progenitor cells ; Endothelial Progenitor Cells - pathology ; Endothelial Progenitor Cells - physiology ; Female ; Humans ; Hypertension ; Hypertension - genetics ; Hypertension - metabolism ; Hypertension - pathology ; Long noncoding RNA p21 ; Male ; Middle Aged ; Nuclear Proteins - metabolism ; Rats ; Rats, Inbred SHR ; Rats, Wistar ; RNA, Long Noncoding ; Tuberous Sclerosis Complex 2 Protein - metabolism ; Vascular Repair</subject><ispartof>Pharmacological research, 2021-11, Vol.173, p.105920-105920, Article 105920</ispartof><rights>2021 The Authors</rights><rights>Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c400t-10ae4367600f88f3f44ce1642f0e56507d4431755c60e2ad1d50494711479ff23</citedby><cites>FETCH-LOGICAL-c400t-10ae4367600f88f3f44ce1642f0e56507d4431755c60e2ad1d50494711479ff23</cites><orcidid>0000-0002-2129-1447</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.phrs.2021.105920$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3549,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34601081$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Chao</creatorcontrib><creatorcontrib>Lin, Lin</creatorcontrib><creatorcontrib>Zhang, Lei</creatorcontrib><creatorcontrib>Xu, Ran</creatorcontrib><creatorcontrib>Chen, Xiaoqing</creatorcontrib><creatorcontrib>Ji, Jingkang</creatorcontrib><creatorcontrib>Li, Yunlun</creatorcontrib><title>Long noncoding RNA p21 enhances autophagy to alleviate endothelial progenitor cells damage and promote endothelial repair in hypertension through SESN2/AMPK/TSC2 pathway</title><title>Pharmacological research</title><addtitle>Pharmacol Res</addtitle><description>Vascular damage of hypertension has been the focus of hypertension treatment, and endothelial progenitor cells (EPCs) play an important role in the repair of vascular endothelial damage. Functional damage and decreased number of EPCs are observed in the peripheral circulation of hypertensive patients, but its mechanism is not yet elucidated. Here, we show that the number of EPCs in hypertensive patients is significantly lower than that of normal population, and the cell function decreases with a higher proportion of EPCs at later stages. A decrease in autophagy is responsible for the senescence and damage of EPCs induced by AngII. Moreover, lncRNA-p21 plays a critical regulator role in EPCs’ senescence and dysfunction. Furthermore, lncRNA-p21 activates SESN2/AMPK/TSC2 pathway by promoting the transcriptional activity of p53 and enhances autophagy to protect against AngII-induced EPC damage. The data provide evidence that a reversal of decreased autophagy serves as the protective mechanism of EPC injury in hypertensive patients, and lncRNA-p21 is a new therapeutic target for vascular endothelial repair in hypertension.
[Display omitted]</description><subject>Aged</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Angiotensin II</subject><subject>Animals</subject><subject>Autophagy</subject><subject>beta-Galactosidase - metabolism</subject><subject>Cell Adhesion</subject><subject>Cell Movement</subject><subject>Endothelial progenitor cells</subject><subject>Endothelial Progenitor Cells - pathology</subject><subject>Endothelial Progenitor Cells - physiology</subject><subject>Female</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hypertension - genetics</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - pathology</subject><subject>Long noncoding RNA p21</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Nuclear Proteins - metabolism</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Wistar</subject><subject>RNA, Long Noncoding</subject><subject>Tuberous Sclerosis Complex 2 Protein - metabolism</subject><subject>Vascular Repair</subject><issn>1043-6618</issn><issn>1096-1186</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc9u1DAQhyNERf_AC3BAPnLJ7thxnETisloVqFhaxJazZeJJ4lViB9sp2kfiLZtoCwcOPXnk-eYnj78keUthRYGK9WE1dj6sGDA6X-QVgxfJBYVKpJSW4uVS8ywVgpbnyWUIBwCoOIVXyXnGBVAo6UXyZ-dsS6yztdNmrr7fbsjIKEHbKVtjIGqKbuxUeyTREdX3-GBUxLmvXeywN6ono3ctWhOdJzX2fSBaDapFoqxeeoP7j_c4KuOJsaQ7jugj2mCcJbHzbmo7sr_e37L15uu3L-v7_ZaRUcXutzq-Ts4a1Qd883ReJT8-Xt9vP6e7u083280urTlATCko5JkoBEBTlk3WcF4jFZw1gLnIodCcZ7TI81oAMqWpzoFXvKCUF1XTsOwqeX_KnZ_-a8IQ5WDCspey6KYgWV5UUM6fuqDshNbeheCxkaM3g_JHSUEuiuRBLorkokieFM1D757yp58D6n8jf53MwIcTgPOWDwa9DLXBWYY2HusotTPP5T8CzAGjRw</recordid><startdate>202111</startdate><enddate>202111</enddate><creator>Li, Chao</creator><creator>Lin, Lin</creator><creator>Zhang, Lei</creator><creator>Xu, Ran</creator><creator>Chen, Xiaoqing</creator><creator>Ji, Jingkang</creator><creator>Li, Yunlun</creator><general>Elsevier Ltd</general><scope>6I.</scope><scope>AAFTH</scope><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><orcidid>https://orcid.org/0000-0002-2129-1447</orcidid></search><sort><creationdate>202111</creationdate><title>Long noncoding RNA p21 enhances autophagy to alleviate endothelial progenitor cells damage and promote endothelial repair in hypertension through SESN2/AMPK/TSC2 pathway</title><author>Li, Chao ; Lin, Lin ; Zhang, Lei ; Xu, Ran ; Chen, Xiaoqing ; Ji, Jingkang ; Li, Yunlun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c400t-10ae4367600f88f3f44ce1642f0e56507d4431755c60e2ad1d50494711479ff23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Aged</topic><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>Angiotensin II</topic><topic>Animals</topic><topic>Autophagy</topic><topic>beta-Galactosidase - metabolism</topic><topic>Cell Adhesion</topic><topic>Cell Movement</topic><topic>Endothelial progenitor cells</topic><topic>Endothelial Progenitor Cells - pathology</topic><topic>Endothelial Progenitor Cells - physiology</topic><topic>Female</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Hypertension - genetics</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - pathology</topic><topic>Long noncoding RNA p21</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Nuclear Proteins - metabolism</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Wistar</topic><topic>RNA, Long Noncoding</topic><topic>Tuberous Sclerosis Complex 2 Protein - metabolism</topic><topic>Vascular Repair</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Chao</creatorcontrib><creatorcontrib>Lin, Lin</creatorcontrib><creatorcontrib>Zhang, Lei</creatorcontrib><creatorcontrib>Xu, Ran</creatorcontrib><creatorcontrib>Chen, Xiaoqing</creatorcontrib><creatorcontrib>Ji, Jingkang</creatorcontrib><creatorcontrib>Li, Yunlun</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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><jtitle>Pharmacological research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Chao</au><au>Lin, Lin</au><au>Zhang, Lei</au><au>Xu, Ran</au><au>Chen, Xiaoqing</au><au>Ji, Jingkang</au><au>Li, Yunlun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long noncoding RNA p21 enhances autophagy to alleviate endothelial progenitor cells damage and promote endothelial repair in hypertension through SESN2/AMPK/TSC2 pathway</atitle><jtitle>Pharmacological research</jtitle><addtitle>Pharmacol Res</addtitle><date>2021-11</date><risdate>2021</risdate><volume>173</volume><spage>105920</spage><epage>105920</epage><pages>105920-105920</pages><artnum>105920</artnum><issn>1043-6618</issn><eissn>1096-1186</eissn><abstract>Vascular damage of hypertension has been the focus of hypertension treatment, and endothelial progenitor cells (EPCs) play an important role in the repair of vascular endothelial damage. Functional damage and decreased number of EPCs are observed in the peripheral circulation of hypertensive patients, but its mechanism is not yet elucidated. Here, we show that the number of EPCs in hypertensive patients is significantly lower than that of normal population, and the cell function decreases with a higher proportion of EPCs at later stages. A decrease in autophagy is responsible for the senescence and damage of EPCs induced by AngII. Moreover, lncRNA-p21 plays a critical regulator role in EPCs’ senescence and dysfunction. Furthermore, lncRNA-p21 activates SESN2/AMPK/TSC2 pathway by promoting the transcriptional activity of p53 and enhances autophagy to protect against AngII-induced EPC damage. The data provide evidence that a reversal of decreased autophagy serves as the protective mechanism of EPC injury in hypertensive patients, and lncRNA-p21 is a new therapeutic target for vascular endothelial repair in hypertension.
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| subjects | Aged AMP-Activated Protein Kinases - metabolism Angiotensin II Animals Autophagy beta-Galactosidase - metabolism Cell Adhesion Cell Movement Endothelial progenitor cells Endothelial Progenitor Cells - pathology Endothelial Progenitor Cells - physiology Female Humans Hypertension Hypertension - genetics Hypertension - metabolism Hypertension - pathology Long noncoding RNA p21 Male Middle Aged Nuclear Proteins - metabolism Rats Rats, Inbred SHR Rats, Wistar RNA, Long Noncoding Tuberous Sclerosis Complex 2 Protein - metabolism Vascular Repair |
| title | Long noncoding RNA p21 enhances autophagy to alleviate endothelial progenitor cells damage and promote endothelial repair in hypertension through SESN2/AMPK/TSC2 pathway |
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