Long noncoding RNA H19 act as a competing endogenous RNA of Let‐7g to facilitate IEC‐6 cell migration and proliferation via regulating EGF

Intestinal mucosal injury is one of the most significant complications of burns. In our previous study, it was found that autophagy could alleviate burn‐induced intestinal injury, but the underlying mechanisms are still unclear. Irregular expression of long noncoding RNAs (lncRNAs) is present in man...

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Veröffentlicht in:Journal of cellular physiology 2021-04, Vol.236 (4), p.2881-2892
Hauptverfasser: Li, Cuijie, Li, Ye, Zhuang, Mengmeng, Zhu, Bo, Zhang, Wenwen, Yan, Hao, Zhang, Pan, Li, Dan, Yang, Juan, Sun, Yuan, Cui, Qingwei, Chen, Haijun, Jin, Peisheng, Xia, Zhaofan, Sun, Yong
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container_issue 4
container_start_page 2881
container_title Journal of cellular physiology
container_volume 236
creator Li, Cuijie
Li, Ye
Zhuang, Mengmeng
Zhu, Bo
Zhang, Wenwen
Yan, Hao
Zhang, Pan
Li, Dan
Yang, Juan
Sun, Yuan
Cui, Qingwei
Chen, Haijun
Jin, Peisheng
Xia, Zhaofan
Sun, Yong
description Intestinal mucosal injury is one of the most significant complications of burns. In our previous study, it was found that autophagy could alleviate burn‐induced intestinal injury, but the underlying mechanisms are still unclear. Irregular expression of long noncoding RNAs (lncRNAs) is present in many diseases, including burns. However, the relationship between lncRNAs and intestinal mucosal injury requires further elucidation. In this study, we established a burn mice model and detected the expression level of autophagy‐related proteins. Then, H19 content after autophagy intervention was tested in vitro and in vivo. The interaction of H19 with Let‐7g and that of Let‐7g with epidermal growth factor (EGF) were verified by dual‐luciferase reporter assays. We found that the expression of the autophagy‐associated proteins LC3‐II and Beclin‐1 was raised in the intestinal tract of the burn mice model. Similarly, the transfection of H19 raised autophagy levels. H19 was elevated after autophagy intervention in vitro and in vivo. H19 overexpression was able to promote IEC‐6 cell migration and proliferation. Let‐7g was suppressed by the overexpression of H19 and the combination of Let‐7g mimic was able to abolish the physiological effect of H19. Moreover, the suppression of Let‐7g increased the expression of EGF protein, which heightened IEC‐6 cell migration and proliferation. Besides this, dual‐luciferase assays revealed that Let‐7g was a direct target of H19 as well as the EGF gene. Taken together, autophagy‐mediated H19 increases in mouse intestinal tract after severe burn and functions as a sponge to Let‐7g to regulate EGF, which suggests that H19 serves as a potential therapeutic target and biomarker for intestinal mucosal injury after burns. Autophagy‐mediated H19 increases in the mouse intestinal tract after severe burn and functions as a sponge to Let‐7g to regulate epidermal growth factor (EGF), which suggests that H19 serves as a potential therapeutic target and biomarker for intestinal mucosal injury after burns.
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In our previous study, it was found that autophagy could alleviate burn‐induced intestinal injury, but the underlying mechanisms are still unclear. Irregular expression of long noncoding RNAs (lncRNAs) is present in many diseases, including burns. However, the relationship between lncRNAs and intestinal mucosal injury requires further elucidation. In this study, we established a burn mice model and detected the expression level of autophagy‐related proteins. Then, H19 content after autophagy intervention was tested in vitro and in vivo. The interaction of H19 with Let‐7g and that of Let‐7g with epidermal growth factor (EGF) were verified by dual‐luciferase reporter assays. We found that the expression of the autophagy‐associated proteins LC3‐II and Beclin‐1 was raised in the intestinal tract of the burn mice model. Similarly, the transfection of H19 raised autophagy levels. H19 was elevated after autophagy intervention in vitro and in vivo. H19 overexpression was able to promote IEC‐6 cell migration and proliferation. Let‐7g was suppressed by the overexpression of H19 and the combination of Let‐7g mimic was able to abolish the physiological effect of H19. Moreover, the suppression of Let‐7g increased the expression of EGF protein, which heightened IEC‐6 cell migration and proliferation. Besides this, dual‐luciferase assays revealed that Let‐7g was a direct target of H19 as well as the EGF gene. Taken together, autophagy‐mediated H19 increases in mouse intestinal tract after severe burn and functions as a sponge to Let‐7g to regulate EGF, which suggests that H19 serves as a potential therapeutic target and biomarker for intestinal mucosal injury after burns. Autophagy‐mediated H19 increases in the mouse intestinal tract after severe burn and functions as a sponge to Let‐7g to regulate epidermal growth factor (EGF), which suggests that H19 serves as a potential therapeutic target and biomarker for intestinal mucosal injury after burns.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.30061</identifier><identifier>PMID: 33230843</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Animals ; Autophagy ; Autophagy-Related Proteins - genetics ; Autophagy-Related Proteins - metabolism ; Biomarkers ; burn ; Burns ; Burns - genetics ; Burns - metabolism ; Burns - pathology ; Cell adhesion &amp; migration ; Cell Line ; Cell migration ; Cell Movement ; Cell Proliferation ; Disease Models, Animal ; Epidermal growth factor ; Epidermal Growth Factor - genetics ; Epidermal Growth Factor - metabolism ; Gene Expression Regulation ; Growth factors ; H19 ; Injuries ; intestinal mucosa ; Intestinal Mucosa - metabolism ; Intestinal Mucosa - pathology ; Intestine ; Let‐7g ; Mice ; Mice, Inbred C57BL ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Mucosa ; Phagocytosis ; Physiological effects ; Proteins ; Rats ; Ribonucleic acid ; RNA ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Signal Transduction ; Therapeutic targets ; Transfection</subject><ispartof>Journal of cellular physiology, 2021-04, Vol.236 (4), p.2881-2892</ispartof><rights>2020 Wiley Periodicals LLC</rights><rights>2020 Wiley Periodicals LLC.</rights><rights>2021 Wiley Periodicals LLC</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3531-aa23fbc70189cb4fadb2bbb9aa5604e3060c3acb1744307d988d31dab6df995a3</citedby><cites>FETCH-LOGICAL-c3531-aa23fbc70189cb4fadb2bbb9aa5604e3060c3acb1744307d988d31dab6df995a3</cites><orcidid>0000-0001-5720-2779</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.30061$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.30061$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33230843$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Cuijie</creatorcontrib><creatorcontrib>Li, Ye</creatorcontrib><creatorcontrib>Zhuang, Mengmeng</creatorcontrib><creatorcontrib>Zhu, Bo</creatorcontrib><creatorcontrib>Zhang, Wenwen</creatorcontrib><creatorcontrib>Yan, Hao</creatorcontrib><creatorcontrib>Zhang, Pan</creatorcontrib><creatorcontrib>Li, Dan</creatorcontrib><creatorcontrib>Yang, Juan</creatorcontrib><creatorcontrib>Sun, Yuan</creatorcontrib><creatorcontrib>Cui, Qingwei</creatorcontrib><creatorcontrib>Chen, Haijun</creatorcontrib><creatorcontrib>Jin, Peisheng</creatorcontrib><creatorcontrib>Xia, Zhaofan</creatorcontrib><creatorcontrib>Sun, Yong</creatorcontrib><title>Long noncoding RNA H19 act as a competing endogenous RNA of Let‐7g to facilitate IEC‐6 cell migration and proliferation via regulating EGF</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>Intestinal mucosal injury is one of the most significant complications of burns. In our previous study, it was found that autophagy could alleviate burn‐induced intestinal injury, but the underlying mechanisms are still unclear. Irregular expression of long noncoding RNAs (lncRNAs) is present in many diseases, including burns. However, the relationship between lncRNAs and intestinal mucosal injury requires further elucidation. In this study, we established a burn mice model and detected the expression level of autophagy‐related proteins. Then, H19 content after autophagy intervention was tested in vitro and in vivo. The interaction of H19 with Let‐7g and that of Let‐7g with epidermal growth factor (EGF) were verified by dual‐luciferase reporter assays. We found that the expression of the autophagy‐associated proteins LC3‐II and Beclin‐1 was raised in the intestinal tract of the burn mice model. Similarly, the transfection of H19 raised autophagy levels. H19 was elevated after autophagy intervention in vitro and in vivo. H19 overexpression was able to promote IEC‐6 cell migration and proliferation. Let‐7g was suppressed by the overexpression of H19 and the combination of Let‐7g mimic was able to abolish the physiological effect of H19. Moreover, the suppression of Let‐7g increased the expression of EGF protein, which heightened IEC‐6 cell migration and proliferation. Besides this, dual‐luciferase assays revealed that Let‐7g was a direct target of H19 as well as the EGF gene. Taken together, autophagy‐mediated H19 increases in mouse intestinal tract after severe burn and functions as a sponge to Let‐7g to regulate EGF, which suggests that H19 serves as a potential therapeutic target and biomarker for intestinal mucosal injury after burns. 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Li, Ye ; Zhuang, Mengmeng ; Zhu, Bo ; Zhang, Wenwen ; Yan, Hao ; Zhang, Pan ; Li, Dan ; Yang, Juan ; Sun, Yuan ; Cui, Qingwei ; Chen, Haijun ; Jin, Peisheng ; Xia, Zhaofan ; Sun, Yong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3531-aa23fbc70189cb4fadb2bbb9aa5604e3060c3acb1744307d988d31dab6df995a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Autophagy</topic><topic>Autophagy-Related Proteins - genetics</topic><topic>Autophagy-Related Proteins - metabolism</topic><topic>Biomarkers</topic><topic>burn</topic><topic>Burns</topic><topic>Burns - genetics</topic><topic>Burns - metabolism</topic><topic>Burns - pathology</topic><topic>Cell adhesion &amp; migration</topic><topic>Cell Line</topic><topic>Cell migration</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Disease Models, Animal</topic><topic>Epidermal growth factor</topic><topic>Epidermal Growth Factor - genetics</topic><topic>Epidermal Growth Factor - metabolism</topic><topic>Gene Expression Regulation</topic><topic>Growth factors</topic><topic>H19</topic><topic>Injuries</topic><topic>intestinal mucosa</topic><topic>Intestinal Mucosa - metabolism</topic><topic>Intestinal Mucosa - pathology</topic><topic>Intestine</topic><topic>Let‐7g</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Mucosa</topic><topic>Phagocytosis</topic><topic>Physiological effects</topic><topic>Proteins</topic><topic>Rats</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Signal Transduction</topic><topic>Therapeutic targets</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Cuijie</creatorcontrib><creatorcontrib>Li, Ye</creatorcontrib><creatorcontrib>Zhuang, Mengmeng</creatorcontrib><creatorcontrib>Zhu, Bo</creatorcontrib><creatorcontrib>Zhang, Wenwen</creatorcontrib><creatorcontrib>Yan, Hao</creatorcontrib><creatorcontrib>Zhang, Pan</creatorcontrib><creatorcontrib>Li, Dan</creatorcontrib><creatorcontrib>Yang, Juan</creatorcontrib><creatorcontrib>Sun, Yuan</creatorcontrib><creatorcontrib>Cui, Qingwei</creatorcontrib><creatorcontrib>Chen, Haijun</creatorcontrib><creatorcontrib>Jin, Peisheng</creatorcontrib><creatorcontrib>Xia, Zhaofan</creatorcontrib><creatorcontrib>Sun, Yong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health &amp; 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In our previous study, it was found that autophagy could alleviate burn‐induced intestinal injury, but the underlying mechanisms are still unclear. Irregular expression of long noncoding RNAs (lncRNAs) is present in many diseases, including burns. However, the relationship between lncRNAs and intestinal mucosal injury requires further elucidation. In this study, we established a burn mice model and detected the expression level of autophagy‐related proteins. Then, H19 content after autophagy intervention was tested in vitro and in vivo. The interaction of H19 with Let‐7g and that of Let‐7g with epidermal growth factor (EGF) were verified by dual‐luciferase reporter assays. We found that the expression of the autophagy‐associated proteins LC3‐II and Beclin‐1 was raised in the intestinal tract of the burn mice model. Similarly, the transfection of H19 raised autophagy levels. H19 was elevated after autophagy intervention in vitro and in vivo. H19 overexpression was able to promote IEC‐6 cell migration and proliferation. Let‐7g was suppressed by the overexpression of H19 and the combination of Let‐7g mimic was able to abolish the physiological effect of H19. Moreover, the suppression of Let‐7g increased the expression of EGF protein, which heightened IEC‐6 cell migration and proliferation. Besides this, dual‐luciferase assays revealed that Let‐7g was a direct target of H19 as well as the EGF gene. Taken together, autophagy‐mediated H19 increases in mouse intestinal tract after severe burn and functions as a sponge to Let‐7g to regulate EGF, which suggests that H19 serves as a potential therapeutic target and biomarker for intestinal mucosal injury after burns. Autophagy‐mediated H19 increases in the mouse intestinal tract after severe burn and functions as a sponge to Let‐7g to regulate epidermal growth factor (EGF), which suggests that H19 serves as a potential therapeutic target and biomarker for intestinal mucosal injury after burns.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>33230843</pmid><doi>10.1002/jcp.30061</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-5720-2779</orcidid></addata></record>
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subjects Animals
Autophagy
Autophagy-Related Proteins - genetics
Autophagy-Related Proteins - metabolism
Biomarkers
burn
Burns
Burns - genetics
Burns - metabolism
Burns - pathology
Cell adhesion & migration
Cell Line
Cell migration
Cell Movement
Cell Proliferation
Disease Models, Animal
Epidermal growth factor
Epidermal Growth Factor - genetics
Epidermal Growth Factor - metabolism
Gene Expression Regulation
Growth factors
H19
Injuries
intestinal mucosa
Intestinal Mucosa - metabolism
Intestinal Mucosa - pathology
Intestine
Let‐7g
Mice
Mice, Inbred C57BL
MicroRNAs - genetics
MicroRNAs - metabolism
Mucosa
Phagocytosis
Physiological effects
Proteins
Rats
Ribonucleic acid
RNA
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Signal Transduction
Therapeutic targets
Transfection
title Long noncoding RNA H19 act as a competing endogenous RNA of Let‐7g to facilitate IEC‐6 cell migration and proliferation via regulating EGF
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