CircRNA_012164/MicroRNA-9-5p axis mediates cardiac fibrosis in diabetic cardiomyopathy
Noncoding RNAs play a part in many chronic diseases and interact with each other to regulate gene expression. MicroRNA-9-5p (miR9) has been thought to be a potential inhibitor of diabetic cardiomyopathy. Here we examined the role of miR9 in regulating cardiac fibrosis in the context of diabetic card...
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| Veröffentlicht in: | PloS one 2024-07, Vol.19 (7), p.e0302772 |
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| description | Noncoding RNAs play a part in many chronic diseases and interact with each other to regulate gene expression. MicroRNA-9-5p (miR9) has been thought to be a potential inhibitor of diabetic cardiomyopathy. Here we examined the role of miR9 in regulating cardiac fibrosis in the context of diabetic cardiomyopathy. We further expanded our studies through investigation of a regulatory circularRNA, circRNA_012164, on the action of miR9. We showed at both the in vivo and in vitro level that glucose induced downregulation of miR9 and upregulation of circRNA_012164 resulted in the subsequent upregulation of downstream fibrotic genes. Further, knockdown of circRNA_012164 shows protective effects in cardiac endothelial cells and reverses increased transcription of genes associated with fibrosis and fibroblast proliferation through a regulatory axis with miR9. This study presents a novel regulatory axis involving noncoding RNA that is evidently important in the development of cardiac fibrosis in diabetic cardiomyopathy. |
| doi_str_mv | 10.1371/journal.pone.0302772 |
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MicroRNA-9-5p (miR9) has been thought to be a potential inhibitor of diabetic cardiomyopathy. Here we examined the role of miR9 in regulating cardiac fibrosis in the context of diabetic cardiomyopathy. We further expanded our studies through investigation of a regulatory circularRNA, circRNA_012164, on the action of miR9. We showed at both the in vivo and in vitro level that glucose induced downregulation of miR9 and upregulation of circRNA_012164 resulted in the subsequent upregulation of downstream fibrotic genes. Further, knockdown of circRNA_012164 shows protective effects in cardiac endothelial cells and reverses increased transcription of genes associated with fibrosis and fibroblast proliferation through a regulatory axis with miR9. This study presents a novel regulatory axis involving noncoding RNA that is evidently important in the development of cardiac fibrosis in diabetic cardiomyopathy.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0302772</identifier><identifier>PMID: 39042659</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Antisense RNA ; Atherosclerosis ; Biology and Life Sciences ; Cardiomyocytes ; Cardiomyopathy ; Cardiovascular disease ; Cell proliferation ; Cell Proliferation - genetics ; Chromosome 5 ; Chronic diseases ; Circular RNA ; Coronary artery disease ; Coronary vessels ; Dextrose ; Diabetes ; Diabetes mellitus ; Diabetic Cardiomyopathies - genetics ; Diabetic Cardiomyopathies - metabolism ; Diabetic Cardiomyopathies - pathology ; Diabetic neuropathy ; DNA methylation ; Endothelial cells ; Endothelial Cells - metabolism ; Endothelial Cells - pathology ; Endothelium ; Engineering and Technology ; Epigenetics ; Fibroblasts ; Fibrosis ; Gene expression ; Gene Expression Regulation ; Genes ; Genetic aspects ; Genetic transcription ; Glucose ; Glucose - metabolism ; Heart ; Heart diseases ; Hyperglycemia ; Hypertension ; In vivo methods and tests ; Laboratories ; Male ; Medicine and Health Sciences ; Mice ; Mice, Inbred C57BL ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Myocardium - metabolism ; Myocardium - pathology ; Non-coding RNA ; Oxidative stress ; Physical Sciences ; Rats ; RNA - genetics ; RNA - metabolism ; RNA, Circular - genetics ; RNA, Circular - metabolism ; Type 2 diabetes ; Up-regulation ; Vein & artery diseases</subject><ispartof>PloS one, 2024-07, Vol.19 (7), p.e0302772</ispartof><rights>Copyright: © 2024 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</rights><rights>COPYRIGHT 2024 Public Library of Science</rights><rights>2024 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2024 Wang et al 2024 Wang et al</rights><rights>2024 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c506t-f2d7d81c70144836ea3cbd9cd096fe76f35dce1488a972b71fe2194958c43e293</cites><orcidid>0000-0002-0208-1401 ; 0000-0001-5140-5567</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11265710/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11265710/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39042659$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Honglin</creatorcontrib><creatorcontrib>Wang, Eric Zi Rui</creatorcontrib><creatorcontrib>Feng, Biao</creatorcontrib><creatorcontrib>Chakrabarti, Subrata</creatorcontrib><title>CircRNA_012164/MicroRNA-9-5p axis mediates cardiac fibrosis in diabetic cardiomyopathy</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Noncoding RNAs play a part in many chronic diseases and interact with each other to regulate gene expression. MicroRNA-9-5p (miR9) has been thought to be a potential inhibitor of diabetic cardiomyopathy. Here we examined the role of miR9 in regulating cardiac fibrosis in the context of diabetic cardiomyopathy. We further expanded our studies through investigation of a regulatory circularRNA, circRNA_012164, on the action of miR9. We showed at both the in vivo and in vitro level that glucose induced downregulation of miR9 and upregulation of circRNA_012164 resulted in the subsequent upregulation of downstream fibrotic genes. Further, knockdown of circRNA_012164 shows protective effects in cardiac endothelial cells and reverses increased transcription of genes associated with fibrosis and fibroblast proliferation through a regulatory axis with miR9. This study presents a novel regulatory axis involving noncoding RNA that is evidently important in the development of cardiac fibrosis in diabetic cardiomyopathy.</description><subject>Animals</subject><subject>Antisense RNA</subject><subject>Atherosclerosis</subject><subject>Biology and Life Sciences</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathy</subject><subject>Cardiovascular disease</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Chromosome 5</subject><subject>Chronic diseases</subject><subject>Circular RNA</subject><subject>Coronary artery disease</subject><subject>Coronary vessels</subject><subject>Dextrose</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetic Cardiomyopathies - genetics</subject><subject>Diabetic Cardiomyopathies - metabolism</subject><subject>Diabetic Cardiomyopathies - pathology</subject><subject>Diabetic neuropathy</subject><subject>DNA methylation</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - pathology</subject><subject>Endothelium</subject><subject>Engineering and Technology</subject><subject>Epigenetics</subject><subject>Fibroblasts</subject><subject>Fibrosis</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic transcription</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Heart</subject><subject>Heart diseases</subject><subject>Hyperglycemia</subject><subject>Hypertension</subject><subject>In vivo methods and tests</subject><subject>Laboratories</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Non-coding RNA</subject><subject>Oxidative stress</subject><subject>Physical Sciences</subject><subject>Rats</subject><subject>RNA - genetics</subject><subject>RNA - metabolism</subject><subject>RNA, Circular - genetics</subject><subject>RNA, Circular - metabolism</subject><subject>Type 2 diabetes</subject><subject>Up-regulation</subject><subject>Vein & artery diseases</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkk1v1DAQhiMEoqXwDxBEQkJwyNZfie0TWq0KVCpUKtCr5Tj2rqskDraDuv--XjatNqgH5IPHM8_M2OM3y15DsICYwtMbN_petovB9XoBMECUoifZMeQYFRUC-OmBfZS9COEGgBKzqnqeHWEOCKpKfpxdr6xXV9-XAkAEK3L6zSrv0rngRTnk8taGvNONlVGHXEmfLJUbW3sXUsT2eXLUOlq1D7pu6wYZN9uX2TMj26BfTftJ9uvz2c_V1-Li8sv5anlRqBJUsTCooQ2DigJICMOVlljVDVcN4JXRtDK4bJSGhDHJKaopNBpBTnjJFMEacXySvd3XHVoXxDSSIDBgmJUIQJaITxMx1uklSvfRy1YM3nbSb4WTVswjvd2ItfsjIEwTohCkCh-mCt79HnWIorNB6baVvXbj32YEIAYRTei7f9DHrzRRa9lqYXvjUmO1KyqWDCCMCcK7totHqLQa3VmVPt3Y5J8lfJwlJCbq27iWYwji_MfV_7OX13P2_QG70bKNm-DaMVrXhzlI9mCSUAhem4cpQyB2mr2fhthpVkyaTWlvDn_oIelepPgOPvHkKA</recordid><startdate>20240723</startdate><enddate>20240723</enddate><creator>Wang, Honglin</creator><creator>Wang, Eric Zi Rui</creator><creator>Feng, Biao</creator><creator>Chakrabarti, Subrata</creator><general>Public Library of Science</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0208-1401</orcidid><orcidid>https://orcid.org/0000-0001-5140-5567</orcidid></search><sort><creationdate>20240723</creationdate><title>CircRNA_012164/MicroRNA-9-5p axis mediates cardiac fibrosis in diabetic cardiomyopathy</title><author>Wang, Honglin ; Wang, Eric Zi Rui ; Feng, Biao ; Chakrabarti, Subrata</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c506t-f2d7d81c70144836ea3cbd9cd096fe76f35dce1488a972b71fe2194958c43e293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Antisense RNA</topic><topic>Atherosclerosis</topic><topic>Biology and Life Sciences</topic><topic>Cardiomyocytes</topic><topic>Cardiomyopathy</topic><topic>Cardiovascular disease</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Chromosome 5</topic><topic>Chronic diseases</topic><topic>Circular RNA</topic><topic>Coronary artery disease</topic><topic>Coronary vessels</topic><topic>Dextrose</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetic Cardiomyopathies - genetics</topic><topic>Diabetic Cardiomyopathies - metabolism</topic><topic>Diabetic Cardiomyopathies - pathology</topic><topic>Diabetic neuropathy</topic><topic>DNA methylation</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelial Cells - pathology</topic><topic>Endothelium</topic><topic>Engineering and Technology</topic><topic>Epigenetics</topic><topic>Fibroblasts</topic><topic>Fibrosis</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic transcription</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Heart</topic><topic>Heart diseases</topic><topic>Hyperglycemia</topic><topic>Hypertension</topic><topic>In vivo methods and tests</topic><topic>Laboratories</topic><topic>Male</topic><topic>Medicine and Health Sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Honglin</au><au>Wang, Eric Zi Rui</au><au>Feng, Biao</au><au>Chakrabarti, Subrata</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CircRNA_012164/MicroRNA-9-5p axis mediates cardiac fibrosis in diabetic cardiomyopathy</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2024-07-23</date><risdate>2024</risdate><volume>19</volume><issue>7</issue><spage>e0302772</spage><pages>e0302772-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Noncoding RNAs play a part in many chronic diseases and interact with each other to regulate gene expression. MicroRNA-9-5p (miR9) has been thought to be a potential inhibitor of diabetic cardiomyopathy. Here we examined the role of miR9 in regulating cardiac fibrosis in the context of diabetic cardiomyopathy. We further expanded our studies through investigation of a regulatory circularRNA, circRNA_012164, on the action of miR9. We showed at both the in vivo and in vitro level that glucose induced downregulation of miR9 and upregulation of circRNA_012164 resulted in the subsequent upregulation of downstream fibrotic genes. Further, knockdown of circRNA_012164 shows protective effects in cardiac endothelial cells and reverses increased transcription of genes associated with fibrosis and fibroblast proliferation through a regulatory axis with miR9. This study presents a novel regulatory axis involving noncoding RNA that is evidently important in the development of cardiac fibrosis in diabetic cardiomyopathy.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>39042659</pmid><doi>10.1371/journal.pone.0302772</doi><tpages>e0302772</tpages><orcidid>https://orcid.org/0000-0002-0208-1401</orcidid><orcidid>https://orcid.org/0000-0001-5140-5567</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antisense RNA Atherosclerosis Biology and Life Sciences Cardiomyocytes Cardiomyopathy Cardiovascular disease Cell proliferation Cell Proliferation - genetics Chromosome 5 Chronic diseases Circular RNA Coronary artery disease Coronary vessels Dextrose Diabetes Diabetes mellitus Diabetic Cardiomyopathies - genetics Diabetic Cardiomyopathies - metabolism Diabetic Cardiomyopathies - pathology Diabetic neuropathy DNA methylation Endothelial cells Endothelial Cells - metabolism Endothelial Cells - pathology Endothelium Engineering and Technology Epigenetics Fibroblasts Fibrosis Gene expression Gene Expression Regulation Genes Genetic aspects Genetic transcription Glucose Glucose - metabolism Heart Heart diseases Hyperglycemia Hypertension In vivo methods and tests Laboratories Male Medicine and Health Sciences Mice Mice, Inbred C57BL MicroRNA MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Myocardium - metabolism Myocardium - pathology Non-coding RNA Oxidative stress Physical Sciences Rats RNA - genetics RNA - metabolism RNA, Circular - genetics RNA, Circular - metabolism Type 2 diabetes Up-regulation Vein & artery diseases |
| title | CircRNA_012164/MicroRNA-9-5p axis mediates cardiac fibrosis in diabetic cardiomyopathy |
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