The lncRNA ADAMTS9-AS1/miR-185-5p/KAT7 ceRNA network inhibits cardiomyocyte hypertrophy in hypertrophic obstructive cardiomyopathy
Hypertrophic obstructive cardiomyopathy (HOCM) is a well-recognized inherited cardiac disease. This study was conducted to explore the role of lncRNA ADAMTS9 antisense RNA 1 (ADAMTS9-AS1) in HOCM-induced cardiomyocyte hypertrophy. The serum of HOCM patients was collected. AC16 cells were treated wit...
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Veröffentlicht in: | Biomedical Research 2023/06/01, Vol.44(3), pp.105-115 |
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description | Hypertrophic obstructive cardiomyopathy (HOCM) is a well-recognized inherited cardiac disease. This study was conducted to explore the role of lncRNA ADAMTS9 antisense RNA 1 (ADAMTS9-AS1) in HOCM-induced cardiomyocyte hypertrophy. The serum of HOCM patients was collected. AC16 cells were treated with isoproterenol (ISO) and transfected with oe-ADAMTS9-AS1 vector, miR-185-5p mimic, and lysine acetyltransferase 7 (KAT7) specific small interfering RNA. lncRNA ADAMTS9-AS1, miR-185-5p, KAT7, brain natriuretic peptide (BNP), and atrial natriuretic peptide (ANP) in the serum or cells were determine by qRT-PCR or Western blot assay. Cell surface area was observed by Texas Red-Phalloidin staining. Subcellular localization of lncRNA ADAMTS9-AS1 was tested by nuclear/cytoplasmic fractionation assay, with RNA pull-down and dual-luciferase assay to validate gene interactions. lncRNA ADAMTS9-AS1 was downregulated in the serum of HOCM patients and ISO-treated AC16 cells. lncRNA ADAMTS9-AS1 overexpression inhibited ISO-induced cardiomyocyte hypertrophy and reduced levels of ANP and BNP. lncRNA ADAMTS9- AS1 was located in cytoplasm and inhibited miR-185-5p expression through targeted binding. miR-185-5p bound to KAT7 3’UTR and inhibited KAT7 expression. miR-185-5p overexpression and KAT7 knockdown both neutralized the inhibitory role of lncRNA ADAMTS9-AS1 in cardiomyocyte hypertrophy. Overall, lncRNA ADAMTS9-AS competitively bound to miR-185-5p to up-regulate KAT7 and thus inhibited cardiomyocyte hypertrophy. |
doi_str_mv | 10.2220/biomedres.44.105 |
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This study was conducted to explore the role of lncRNA ADAMTS9 antisense RNA 1 (ADAMTS9-AS1) in HOCM-induced cardiomyocyte hypertrophy. The serum of HOCM patients was collected. AC16 cells were treated with isoproterenol (ISO) and transfected with oe-ADAMTS9-AS1 vector, miR-185-5p mimic, and lysine acetyltransferase 7 (KAT7) specific small interfering RNA. lncRNA ADAMTS9-AS1, miR-185-5p, KAT7, brain natriuretic peptide (BNP), and atrial natriuretic peptide (ANP) in the serum or cells were determine by qRT-PCR or Western blot assay. Cell surface area was observed by Texas Red-Phalloidin staining. Subcellular localization of lncRNA ADAMTS9-AS1 was tested by nuclear/cytoplasmic fractionation assay, with RNA pull-down and dual-luciferase assay to validate gene interactions. lncRNA ADAMTS9-AS1 was downregulated in the serum of HOCM patients and ISO-treated AC16 cells. lncRNA ADAMTS9-AS1 overexpression inhibited ISO-induced cardiomyocyte hypertrophy and reduced levels of ANP and BNP. lncRNA ADAMTS9- AS1 was located in cytoplasm and inhibited miR-185-5p expression through targeted binding. miR-185-5p bound to KAT7 3’UTR and inhibited KAT7 expression. miR-185-5p overexpression and KAT7 knockdown both neutralized the inhibitory role of lncRNA ADAMTS9-AS1 in cardiomyocyte hypertrophy. Overall, lncRNA ADAMTS9-AS competitively bound to miR-185-5p to up-regulate KAT7 and thus inhibited cardiomyocyte hypertrophy.</description><identifier>ISSN: 0388-6107</identifier><identifier>EISSN: 1880-313X</identifier><identifier>DOI: 10.2220/biomedres.44.105</identifier><identifier>PMID: 37258203</identifier><language>eng</language><publisher>Japan: Biomedical Research Press</publisher><subject>3' Untranslated regions ; Acetyltransferase ; Antisense RNA ; Assaying ; Atrial natriuretic peptide ; Brain natriuretic peptide ; Cardiomyocytes ; Cardiomyopathy ; Cell surface ; Coronary artery disease ; Cytoplasm ; Fractionation ; Heart diseases ; Hypertrophy ; Localization ; Lysine ; Non-coding RNA ; Peptides ; Phalloidin ; Ribonucleic acid ; RNA ; siRNA</subject><ispartof>Biomedical Research, 2023/06/01, Vol.44(3), pp.105-115</ispartof><rights>2023 Biomedical Research Press</rights><rights>Copyright Japan Science and Technology Agency 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c506t-63fd977a7089e39c6b991475cb4f54e4c848b0afc21504b6d648144cf7d7afbb3</citedby><cites>FETCH-LOGICAL-c506t-63fd977a7089e39c6b991475cb4f54e4c848b0afc21504b6d648144cf7d7afbb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1883,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37258203$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SONG, Bangrong</creatorcontrib><creatorcontrib>LI, Wei</creatorcontrib><creatorcontrib>XU, Xiaoyu</creatorcontrib><creatorcontrib>DANG, Haiming</creatorcontrib><creatorcontrib>DONG, Ran</creatorcontrib><title>The lncRNA ADAMTS9-AS1/miR-185-5p/KAT7 ceRNA network inhibits cardiomyocyte hypertrophy in hypertrophic obstructive cardiomyopathy</title><title>Biomedical Research</title><addtitle>Biomed. Res.</addtitle><description>Hypertrophic obstructive cardiomyopathy (HOCM) is a well-recognized inherited cardiac disease. This study was conducted to explore the role of lncRNA ADAMTS9 antisense RNA 1 (ADAMTS9-AS1) in HOCM-induced cardiomyocyte hypertrophy. The serum of HOCM patients was collected. AC16 cells were treated with isoproterenol (ISO) and transfected with oe-ADAMTS9-AS1 vector, miR-185-5p mimic, and lysine acetyltransferase 7 (KAT7) specific small interfering RNA. lncRNA ADAMTS9-AS1, miR-185-5p, KAT7, brain natriuretic peptide (BNP), and atrial natriuretic peptide (ANP) in the serum or cells were determine by qRT-PCR or Western blot assay. Cell surface area was observed by Texas Red-Phalloidin staining. Subcellular localization of lncRNA ADAMTS9-AS1 was tested by nuclear/cytoplasmic fractionation assay, with RNA pull-down and dual-luciferase assay to validate gene interactions. lncRNA ADAMTS9-AS1 was downregulated in the serum of HOCM patients and ISO-treated AC16 cells. lncRNA ADAMTS9-AS1 overexpression inhibited ISO-induced cardiomyocyte hypertrophy and reduced levels of ANP and BNP. lncRNA ADAMTS9- AS1 was located in cytoplasm and inhibited miR-185-5p expression through targeted binding. miR-185-5p bound to KAT7 3’UTR and inhibited KAT7 expression. miR-185-5p overexpression and KAT7 knockdown both neutralized the inhibitory role of lncRNA ADAMTS9-AS1 in cardiomyocyte hypertrophy. Overall, lncRNA ADAMTS9-AS competitively bound to miR-185-5p to up-regulate KAT7 and thus inhibited cardiomyocyte hypertrophy.</description><subject>3' Untranslated regions</subject><subject>Acetyltransferase</subject><subject>Antisense RNA</subject><subject>Assaying</subject><subject>Atrial natriuretic peptide</subject><subject>Brain natriuretic peptide</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathy</subject><subject>Cell surface</subject><subject>Coronary artery disease</subject><subject>Cytoplasm</subject><subject>Fractionation</subject><subject>Heart diseases</subject><subject>Hypertrophy</subject><subject>Localization</subject><subject>Lysine</subject><subject>Non-coding RNA</subject><subject>Peptides</subject><subject>Phalloidin</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>siRNA</subject><issn>0388-6107</issn><issn>1880-313X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNpdkUuP0zAURi0EYsrAnhWKxIZNWr_tLKPyFANIM0ViF9mOQ1zSOGM7oGz55XjUUh4r6_qe7-hKHwBPEVxjjOFGO3-wbbBxTekaQXYPrJCUsCSIfLkPVpBIWXIExQV4FOMe5hlJ8hBcEIGZxJCswM9db4thNNcf66J-WX_Y3VRlfYM2B3ddIslKNm3e1ztRGHtHjDb98OFb4cbeaZdiYVRo8w2LN0uyRb9MNqTgp37JyF-jM4XXMYXZJPfd_klNKvXLY_CgU0O0T07vJfj8-tVu-7a8-vTm3ba-Kg2DPJWcdG0lhBJQVpZUhuuqQlQwo2nHqKVGUqmh6gxGDFLNW04lotR0ohWq05pcghdH7xT87Wxjag4uGjsMarR-jg2WGHGKiaQZff4fuvdzGPN1mcp2TjCXmYJHygQfY7BdMwV3UGFpEGzu-mnO_TSU5k-WI89O4lnnzTnwu5AMbI_APib11Z4BFZIzg_3XSE7a89b0KjR2JL8AUwSmpA</recordid><startdate>20230601</startdate><enddate>20230601</enddate><creator>SONG, Bangrong</creator><creator>LI, Wei</creator><creator>XU, Xiaoyu</creator><creator>DANG, Haiming</creator><creator>DONG, Ran</creator><general>Biomedical Research Press</general><general>Japan Science and Technology Agency</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7QP</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20230601</creationdate><title>The lncRNA ADAMTS9-AS1/miR-185-5p/KAT7 ceRNA network inhibits cardiomyocyte hypertrophy in hypertrophic obstructive cardiomyopathy</title><author>SONG, Bangrong ; LI, Wei ; XU, Xiaoyu ; DANG, Haiming ; DONG, Ran</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c506t-63fd977a7089e39c6b991475cb4f54e4c848b0afc21504b6d648144cf7d7afbb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>3' Untranslated regions</topic><topic>Acetyltransferase</topic><topic>Antisense RNA</topic><topic>Assaying</topic><topic>Atrial natriuretic peptide</topic><topic>Brain natriuretic peptide</topic><topic>Cardiomyocytes</topic><topic>Cardiomyopathy</topic><topic>Cell surface</topic><topic>Coronary artery disease</topic><topic>Cytoplasm</topic><topic>Fractionation</topic><topic>Heart diseases</topic><topic>Hypertrophy</topic><topic>Localization</topic><topic>Lysine</topic><topic>Non-coding RNA</topic><topic>Peptides</topic><topic>Phalloidin</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>siRNA</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SONG, Bangrong</creatorcontrib><creatorcontrib>LI, Wei</creatorcontrib><creatorcontrib>XU, Xiaoyu</creatorcontrib><creatorcontrib>DANG, Haiming</creatorcontrib><creatorcontrib>DONG, Ran</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biomedical Research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SONG, Bangrong</au><au>LI, Wei</au><au>XU, Xiaoyu</au><au>DANG, Haiming</au><au>DONG, Ran</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The lncRNA ADAMTS9-AS1/miR-185-5p/KAT7 ceRNA network inhibits cardiomyocyte hypertrophy in hypertrophic obstructive cardiomyopathy</atitle><jtitle>Biomedical Research</jtitle><addtitle>Biomed. Res.</addtitle><date>2023-06-01</date><risdate>2023</risdate><volume>44</volume><issue>3</issue><spage>105</spage><epage>115</epage><pages>105-115</pages><issn>0388-6107</issn><eissn>1880-313X</eissn><abstract>Hypertrophic obstructive cardiomyopathy (HOCM) is a well-recognized inherited cardiac disease. This study was conducted to explore the role of lncRNA ADAMTS9 antisense RNA 1 (ADAMTS9-AS1) in HOCM-induced cardiomyocyte hypertrophy. The serum of HOCM patients was collected. AC16 cells were treated with isoproterenol (ISO) and transfected with oe-ADAMTS9-AS1 vector, miR-185-5p mimic, and lysine acetyltransferase 7 (KAT7) specific small interfering RNA. lncRNA ADAMTS9-AS1, miR-185-5p, KAT7, brain natriuretic peptide (BNP), and atrial natriuretic peptide (ANP) in the serum or cells were determine by qRT-PCR or Western blot assay. Cell surface area was observed by Texas Red-Phalloidin staining. Subcellular localization of lncRNA ADAMTS9-AS1 was tested by nuclear/cytoplasmic fractionation assay, with RNA pull-down and dual-luciferase assay to validate gene interactions. lncRNA ADAMTS9-AS1 was downregulated in the serum of HOCM patients and ISO-treated AC16 cells. lncRNA ADAMTS9-AS1 overexpression inhibited ISO-induced cardiomyocyte hypertrophy and reduced levels of ANP and BNP. lncRNA ADAMTS9- AS1 was located in cytoplasm and inhibited miR-185-5p expression through targeted binding. miR-185-5p bound to KAT7 3’UTR and inhibited KAT7 expression. miR-185-5p overexpression and KAT7 knockdown both neutralized the inhibitory role of lncRNA ADAMTS9-AS1 in cardiomyocyte hypertrophy. Overall, lncRNA ADAMTS9-AS competitively bound to miR-185-5p to up-regulate KAT7 and thus inhibited cardiomyocyte hypertrophy.</abstract><cop>Japan</cop><pub>Biomedical Research Press</pub><pmid>37258203</pmid><doi>10.2220/biomedres.44.105</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 3' Untranslated regions Acetyltransferase Antisense RNA Assaying Atrial natriuretic peptide Brain natriuretic peptide Cardiomyocytes Cardiomyopathy Cell surface Coronary artery disease Cytoplasm Fractionation Heart diseases Hypertrophy Localization Lysine Non-coding RNA Peptides Phalloidin Ribonucleic acid RNA siRNA |
title | The lncRNA ADAMTS9-AS1/miR-185-5p/KAT7 ceRNA network inhibits cardiomyocyte hypertrophy in hypertrophic obstructive cardiomyopathy |
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