LncRNA H19 Inhibits the Progression of Sepsis-Induced Myocardial Injury via Regulation of the miR-93-5p/SORBS2 Axis
Sepsis is an infectious disease that seriously endangers human health. It usually leads to myocardial injury which seriously endangers to the health of human beings. H19 has been confirmed to play key roles in various diseases, including sepsis. However, its function in the progression of sepsis-ind...
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| Veröffentlicht in: | Inflammation 2021-02, Vol.44 (1), p.344-357 |
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| creator | Shan, Bin Li, Jia-Yan Liu, Ya-Jiang Tang, Xiao-Bin Zhou, Zheng Luo, Liang-Xian |
| description | Sepsis is an infectious disease that seriously endangers human health. It usually leads to myocardial injury which seriously endangers to the health of human beings. H19 has been confirmed to play key roles in various diseases, including sepsis. However, its function in the progression of sepsis-induced myocardial injury remains largely unknown. H9C2 cells were treated with lipopolysaccharide (LPS) to mimic sepsis-induced myocardial injury
in vitro
. Cell proliferation and apoptosis were detected by MTT assay and flow cytometry, respectively. In addition, gene and protein expression levels in H9C2 cells were measured by quantitative real-time PCR (qRT-PCR) and Western blotting. The levels of inflammatory cytokines in H9C2 cell supernatants were tested by ELISA. JC-1 staining was performed to observe the mitochondrial membrane potential level in H9C2 cells. H19 and SORBS2 were downregulated in H9C2 cells following LPS treatment, while miR-93-5p was upregulated. Moreover, LPS-induced cell growth inhibition and mitochondrial damage were significantly reversed by overexpression of H19. In addition, H19 upregulation notably suppressed LPS-induced inflammatory responses in H9C2 cells. Moreover, H19 sponged miR-93-5p to promote SORBS2 expression. Overall, H19 suppressed sepsis-induced myocardial injury
via
regulation of the miR-93-5p/SORBS2 axis. H19 attenuated the development of sepsis-induced myocardial injury
in vitro via
modulation of the miR-93-5p/SORBS2 axis. Thus, H19 could serve as a potential target for the treatment of sepsis-induced myocardial injury. |
| doi_str_mv | 10.1007/s10753-020-01340-8 |
| format | Article |
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in vitro
. Cell proliferation and apoptosis were detected by MTT assay and flow cytometry, respectively. In addition, gene and protein expression levels in H9C2 cells were measured by quantitative real-time PCR (qRT-PCR) and Western blotting. The levels of inflammatory cytokines in H9C2 cell supernatants were tested by ELISA. JC-1 staining was performed to observe the mitochondrial membrane potential level in H9C2 cells. H19 and SORBS2 were downregulated in H9C2 cells following LPS treatment, while miR-93-5p was upregulated. Moreover, LPS-induced cell growth inhibition and mitochondrial damage were significantly reversed by overexpression of H19. In addition, H19 upregulation notably suppressed LPS-induced inflammatory responses in H9C2 cells. Moreover, H19 sponged miR-93-5p to promote SORBS2 expression. Overall, H19 suppressed sepsis-induced myocardial injury
via
regulation of the miR-93-5p/SORBS2 axis. H19 attenuated the development of sepsis-induced myocardial injury
in vitro via
modulation of the miR-93-5p/SORBS2 axis. Thus, H19 could serve as a potential target for the treatment of sepsis-induced myocardial injury.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-020-01340-8</identifier><identifier>PMID: 32996061</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Cell growth ; Cell proliferation ; Cytokines ; Enzyme-linked immunosorbent assay ; Flow cytometry ; Immunology ; Infectious diseases ; Inflammation ; Internal Medicine ; Lipopolysaccharides ; Membrane potential ; Mitochondria ; Original Article ; Pathology ; Pharmacology/Toxicology ; Rheumatology ; Sepsis ; Western blotting</subject><ispartof>Inflammation, 2021-02, Vol.44 (1), p.344-357</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2908-30da94a6d5dbfe8cb5596accef9fcbd2d33a60dca3ec8ca11dc989cb6a11a6d23</citedby><cites>FETCH-LOGICAL-c2908-30da94a6d5dbfe8cb5596accef9fcbd2d33a60dca3ec8ca11dc989cb6a11a6d23</cites><orcidid>0000-0002-8384-2304</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10753-020-01340-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10753-020-01340-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32996061$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shan, Bin</creatorcontrib><creatorcontrib>Li, Jia-Yan</creatorcontrib><creatorcontrib>Liu, Ya-Jiang</creatorcontrib><creatorcontrib>Tang, Xiao-Bin</creatorcontrib><creatorcontrib>Zhou, Zheng</creatorcontrib><creatorcontrib>Luo, Liang-Xian</creatorcontrib><title>LncRNA H19 Inhibits the Progression of Sepsis-Induced Myocardial Injury via Regulation of the miR-93-5p/SORBS2 Axis</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>Sepsis is an infectious disease that seriously endangers human health. It usually leads to myocardial injury which seriously endangers to the health of human beings. H19 has been confirmed to play key roles in various diseases, including sepsis. However, its function in the progression of sepsis-induced myocardial injury remains largely unknown. H9C2 cells were treated with lipopolysaccharide (LPS) to mimic sepsis-induced myocardial injury
in vitro
. Cell proliferation and apoptosis were detected by MTT assay and flow cytometry, respectively. In addition, gene and protein expression levels in H9C2 cells were measured by quantitative real-time PCR (qRT-PCR) and Western blotting. The levels of inflammatory cytokines in H9C2 cell supernatants were tested by ELISA. JC-1 staining was performed to observe the mitochondrial membrane potential level in H9C2 cells. H19 and SORBS2 were downregulated in H9C2 cells following LPS treatment, while miR-93-5p was upregulated. Moreover, LPS-induced cell growth inhibition and mitochondrial damage were significantly reversed by overexpression of H19. In addition, H19 upregulation notably suppressed LPS-induced inflammatory responses in H9C2 cells. Moreover, H19 sponged miR-93-5p to promote SORBS2 expression. Overall, H19 suppressed sepsis-induced myocardial injury
via
regulation of the miR-93-5p/SORBS2 axis. H19 attenuated the development of sepsis-induced myocardial injury
in vitro via
modulation of the miR-93-5p/SORBS2 axis. Thus, H19 could serve as a potential target for the treatment of sepsis-induced myocardial injury.</description><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Cytokines</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Flow cytometry</subject><subject>Immunology</subject><subject>Infectious diseases</subject><subject>Inflammation</subject><subject>Internal Medicine</subject><subject>Lipopolysaccharides</subject><subject>Membrane potential</subject><subject>Mitochondria</subject><subject>Original Article</subject><subject>Pathology</subject><subject>Pharmacology/Toxicology</subject><subject>Rheumatology</subject><subject>Sepsis</subject><subject>Western blotting</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kcFOGzEURS3UqqTQH2BRWeqGjcuzPeOxlwFRiJQCStq15bE9wdFkJrUzqPl7nCYFiQUrP8nnnveki9AZhe8UoLpIFKqSE2BAgPICiDxCI1pWnLCyEh_QCLgAwpWqjtHnlJYAIJXkn9AxZ0oJEHSE0rSzs7sxvqUKT7rHUIdNwptHjx9iv4g-pdB3uG_w3K9TSGTSucF6h39ue2uiC6bNqeUQt_gpGDzzi6E1m0NkZ1mFGVGclOuL-f3scs7w-G9Ip-hjY9rkvxzeE_T7x_Wvq1syvb-ZXI2nxDIFknBwRhVGuNLVjZe2LksljLW-UY2tHXOcGwHOGu6ttIZSZ5VUthZ5zCnGT9D53ruO_Z_Bp41ehWR925rO90PSrCiqsmCF5Bn99gZd9kPs8nWZqgSvGFM7IdtTNvYpRd_odQwrE7eagt5VoveV6FyJ_leJljn09aAe6pV3L5H_HWSA74GUv7qFj6-739E-A8L0ldI</recordid><startdate>20210201</startdate><enddate>20210201</enddate><creator>Shan, Bin</creator><creator>Li, Jia-Yan</creator><creator>Liu, Ya-Jiang</creator><creator>Tang, Xiao-Bin</creator><creator>Zhou, Zheng</creator><creator>Luo, Liang-Xian</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8384-2304</orcidid></search><sort><creationdate>20210201</creationdate><title>LncRNA H19 Inhibits the Progression of Sepsis-Induced Myocardial Injury via Regulation of the miR-93-5p/SORBS2 Axis</title><author>Shan, Bin ; Li, Jia-Yan ; Liu, Ya-Jiang ; Tang, Xiao-Bin ; Zhou, Zheng ; Luo, Liang-Xian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2908-30da94a6d5dbfe8cb5596accef9fcbd2d33a60dca3ec8ca11dc989cb6a11a6d23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Cytokines</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Flow cytometry</topic><topic>Immunology</topic><topic>Infectious diseases</topic><topic>Inflammation</topic><topic>Internal Medicine</topic><topic>Lipopolysaccharides</topic><topic>Membrane potential</topic><topic>Mitochondria</topic><topic>Original Article</topic><topic>Pathology</topic><topic>Pharmacology/Toxicology</topic><topic>Rheumatology</topic><topic>Sepsis</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shan, Bin</creatorcontrib><creatorcontrib>Li, Jia-Yan</creatorcontrib><creatorcontrib>Liu, Ya-Jiang</creatorcontrib><creatorcontrib>Tang, Xiao-Bin</creatorcontrib><creatorcontrib>Zhou, Zheng</creatorcontrib><creatorcontrib>Luo, Liang-Xian</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shan, Bin</au><au>Li, Jia-Yan</au><au>Liu, Ya-Jiang</au><au>Tang, Xiao-Bin</au><au>Zhou, Zheng</au><au>Luo, Liang-Xian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LncRNA H19 Inhibits the Progression of Sepsis-Induced Myocardial Injury via Regulation of the miR-93-5p/SORBS2 Axis</atitle><jtitle>Inflammation</jtitle><stitle>Inflammation</stitle><addtitle>Inflammation</addtitle><date>2021-02-01</date><risdate>2021</risdate><volume>44</volume><issue>1</issue><spage>344</spage><epage>357</epage><pages>344-357</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><abstract>Sepsis is an infectious disease that seriously endangers human health. It usually leads to myocardial injury which seriously endangers to the health of human beings. H19 has been confirmed to play key roles in various diseases, including sepsis. However, its function in the progression of sepsis-induced myocardial injury remains largely unknown. H9C2 cells were treated with lipopolysaccharide (LPS) to mimic sepsis-induced myocardial injury
in vitro
. Cell proliferation and apoptosis were detected by MTT assay and flow cytometry, respectively. In addition, gene and protein expression levels in H9C2 cells were measured by quantitative real-time PCR (qRT-PCR) and Western blotting. The levels of inflammatory cytokines in H9C2 cell supernatants were tested by ELISA. JC-1 staining was performed to observe the mitochondrial membrane potential level in H9C2 cells. H19 and SORBS2 were downregulated in H9C2 cells following LPS treatment, while miR-93-5p was upregulated. Moreover, LPS-induced cell growth inhibition and mitochondrial damage were significantly reversed by overexpression of H19. In addition, H19 upregulation notably suppressed LPS-induced inflammatory responses in H9C2 cells. Moreover, H19 sponged miR-93-5p to promote SORBS2 expression. Overall, H19 suppressed sepsis-induced myocardial injury
via
regulation of the miR-93-5p/SORBS2 axis. H19 attenuated the development of sepsis-induced myocardial injury
in vitro via
modulation of the miR-93-5p/SORBS2 axis. Thus, H19 could serve as a potential target for the treatment of sepsis-induced myocardial injury.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>32996061</pmid><doi>10.1007/s10753-020-01340-8</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-8384-2304</orcidid></addata></record> |
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| subjects | Apoptosis Biomedical and Life Sciences Biomedicine Cell growth Cell proliferation Cytokines Enzyme-linked immunosorbent assay Flow cytometry Immunology Infectious diseases Inflammation Internal Medicine Lipopolysaccharides Membrane potential Mitochondria Original Article Pathology Pharmacology/Toxicology Rheumatology Sepsis Western blotting |
| title | LncRNA H19 Inhibits the Progression of Sepsis-Induced Myocardial Injury via Regulation of the miR-93-5p/SORBS2 Axis |
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