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TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner
Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is als...
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| Published in: | Genes 2023-02, Vol.14 (3), p.591 |
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| cites | cdi_FETCH-LOGICAL-c483t-db8475f2bbc595ed5c1c18f59be591070444dbd04b19031fed7082b00d9aea0b3 |
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| container_issue | 3 |
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| creator | Cheng, Hao Li, Linnan Xue, Junqiang Ma, Jianying Ge, Junbo |
| description | Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is also a key regulator of proliferation and apoptosis in cardiomyocytes. As a significant m
A regulator, METTL3 binds m
A sites in mRNA to control its degradation, maturation, stabilization, and translation. Whether METTL3 regulates the occurrence and development of myocardial infarction through the m
A modification of TNC mRNA deserves our study. Here, we have demonstrated that overexpression of METTL3 aggravated cardiac dysfunction and cardiac fibrosis after 4 weeks after MI. Moreover, we also demonstrated that TNC resulted in cardiac fibrosis and cardiomyocyte apoptosis after MI. Mechanistically, METTL3 led to enhanced m
A levels of TNC mRNA and promoted TNC mRNA stability. Then, we mutated one m
A site "A" to "T", and the binding ability of METTL3 was reduced. In conclusion, METTL3 is involved in cardiac fibrosis and cardiomyocyte apoptosis by increasing m
A levels of TNC mRNA and may be a promising target for the therapy of cardiac fibrosis after MI. |
| doi_str_mv | 10.3390/genes14030591 |
| format | article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10048594</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A743765251</galeid><sourcerecordid>A743765251</sourcerecordid><originalsourceid>FETCH-LOGICAL-c483t-db8475f2bbc595ed5c1c18f59be591070444dbd04b19031fed7082b00d9aea0b3</originalsourceid><addsrcrecordid>eNptkk1vEzEQhlcIRKu2R65oJS5ctoy_4vUJRWmhEWl7CWfLH7PB0cYb7Cwi_x5HLaWpsA8e2c-89jueqnpH4JIxBZ9WGDETDgyEIq-qUwqSNZxT8fpZfFJd5LyGMjhQAPG2OmET1UI7YafVt-XdrJ46hz0ms8Nc3-y3w-9gmnn0o0Nfz0zywbh6Htdj2tch1qa-vV4uF6y5wi1Gj3FX35oYMZ1XbzrTZ7x4XM-q71-ul7ObZnH_dT6bLhrHW7ZrvG25FB211gkl0AtHHGk7oSwWFyCBc-6tB26JAkY69BJaagG8MmjAsrPq84PudrQb9K68IJleb1PYmLTXgwn6-CSGH3o1_NKklKAViheFj48Kafg5Yt7pTcilBr2JOIxZU6koV4pLWdAPL9D1MKZY_B0oPuGKSPqPWpkedYjdUC52B1E9lZzJiaCCFOryP1SZHjfBDRG7UPaPEpqHBJeGnBN2TyYJ6EMH6KMOKPz755V5ov_-N_sDBXWpfw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2794649172</pqid></control><display><type>article</type><title>TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner</title><source>PubMed Central Free</source><source>ProQuest - Publicly Available Content Database</source><source>Coronavirus Research Database</source><creator>Cheng, Hao ; Li, Linnan ; Xue, Junqiang ; Ma, Jianying ; Ge, Junbo</creator><creatorcontrib>Cheng, Hao ; Li, Linnan ; Xue, Junqiang ; Ma, Jianying ; Ge, Junbo</creatorcontrib><description>Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is also a key regulator of proliferation and apoptosis in cardiomyocytes. As a significant m
A regulator, METTL3 binds m
A sites in mRNA to control its degradation, maturation, stabilization, and translation. Whether METTL3 regulates the occurrence and development of myocardial infarction through the m
A modification of TNC mRNA deserves our study. Here, we have demonstrated that overexpression of METTL3 aggravated cardiac dysfunction and cardiac fibrosis after 4 weeks after MI. Moreover, we also demonstrated that TNC resulted in cardiac fibrosis and cardiomyocyte apoptosis after MI. Mechanistically, METTL3 led to enhanced m
A levels of TNC mRNA and promoted TNC mRNA stability. Then, we mutated one m
A site "A" to "T", and the binding ability of METTL3 was reduced. In conclusion, METTL3 is involved in cardiac fibrosis and cardiomyocyte apoptosis by increasing m
A levels of TNC mRNA and may be a promising target for the therapy of cardiac fibrosis after MI.</description><identifier>ISSN: 2073-4425</identifier><identifier>EISSN: 2073-4425</identifier><identifier>DOI: 10.3390/genes14030591</identifier><identifier>PMID: 36980863</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Acids ; Animals ; Apoptosis ; Biomarkers ; Cardiac function ; Cardiomyocytes ; Congestive heart failure ; Development and progression ; Estrogens ; Ethanol ; Extracellular matrix ; Extracellular Matrix - metabolism ; Fibrosis ; Genetic aspects ; Glycoproteins ; Health aspects ; Heart attacks ; Heart diseases ; Heart failure ; Heart Injuries - metabolism ; Heart Injuries - pathology ; Hypoxia ; Hypoxia - complications ; Hypoxia - metabolism ; Laboratory animals ; Messenger RNA ; Methyltransferases ; Methyltransferases - genetics ; Methyltransferases - metabolism ; Mice ; mRNA stability ; Myocardial infarction ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocytes, Cardiac - metabolism ; N6-methyladenosine ; Physiology ; RNA modification ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Software ; Tenascin ; Tenascin - genetics ; Tenascin C</subject><ispartof>Genes, 2023-02, Vol.14 (3), p.591</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 by the authors. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-db8475f2bbc595ed5c1c18f59be591070444dbd04b19031fed7082b00d9aea0b3</citedby><cites>FETCH-LOGICAL-c483t-db8475f2bbc595ed5c1c18f59be591070444dbd04b19031fed7082b00d9aea0b3</cites><orcidid>0000-0003-1360-6290</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2794649172/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2794649172?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,38516,43895,44590,53791,53793,74412,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36980863$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cheng, Hao</creatorcontrib><creatorcontrib>Li, Linnan</creatorcontrib><creatorcontrib>Xue, Junqiang</creatorcontrib><creatorcontrib>Ma, Jianying</creatorcontrib><creatorcontrib>Ge, Junbo</creatorcontrib><title>TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner</title><title>Genes</title><addtitle>Genes (Basel)</addtitle><description>Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is also a key regulator of proliferation and apoptosis in cardiomyocytes. As a significant m
A regulator, METTL3 binds m
A sites in mRNA to control its degradation, maturation, stabilization, and translation. Whether METTL3 regulates the occurrence and development of myocardial infarction through the m
A modification of TNC mRNA deserves our study. Here, we have demonstrated that overexpression of METTL3 aggravated cardiac dysfunction and cardiac fibrosis after 4 weeks after MI. Moreover, we also demonstrated that TNC resulted in cardiac fibrosis and cardiomyocyte apoptosis after MI. Mechanistically, METTL3 led to enhanced m
A levels of TNC mRNA and promoted TNC mRNA stability. Then, we mutated one m
A site "A" to "T", and the binding ability of METTL3 was reduced. In conclusion, METTL3 is involved in cardiac fibrosis and cardiomyocyte apoptosis by increasing m
A levels of TNC mRNA and may be a promising target for the therapy of cardiac fibrosis after MI.</description><subject>Acids</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biomarkers</subject><subject>Cardiac function</subject><subject>Cardiomyocytes</subject><subject>Congestive heart failure</subject><subject>Development and progression</subject><subject>Estrogens</subject><subject>Ethanol</subject><subject>Extracellular matrix</subject><subject>Extracellular Matrix - metabolism</subject><subject>Fibrosis</subject><subject>Genetic aspects</subject><subject>Glycoproteins</subject><subject>Health aspects</subject><subject>Heart attacks</subject><subject>Heart diseases</subject><subject>Heart failure</subject><subject>Heart Injuries - metabolism</subject><subject>Heart Injuries - pathology</subject><subject>Hypoxia</subject><subject>Hypoxia - complications</subject><subject>Hypoxia - metabolism</subject><subject>Laboratory animals</subject><subject>Messenger RNA</subject><subject>Methyltransferases</subject><subject>Methyltransferases - genetics</subject><subject>Methyltransferases - metabolism</subject><subject>Mice</subject><subject>mRNA stability</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>N6-methyladenosine</subject><subject>Physiology</subject><subject>RNA modification</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Software</subject><subject>Tenascin</subject><subject>Tenascin - genetics</subject><subject>Tenascin C</subject><issn>2073-4425</issn><issn>2073-4425</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>COVID</sourceid><sourceid>PIMPY</sourceid><recordid>eNptkk1vEzEQhlcIRKu2R65oJS5ctoy_4vUJRWmhEWl7CWfLH7PB0cYb7Cwi_x5HLaWpsA8e2c-89jueqnpH4JIxBZ9WGDETDgyEIq-qUwqSNZxT8fpZfFJd5LyGMjhQAPG2OmET1UI7YafVt-XdrJ46hz0ms8Nc3-y3w-9gmnn0o0Nfz0zywbh6Htdj2tch1qa-vV4uF6y5wi1Gj3FX35oYMZ1XbzrTZ7x4XM-q71-ul7ObZnH_dT6bLhrHW7ZrvG25FB211gkl0AtHHGk7oSwWFyCBc-6tB26JAkY69BJaagG8MmjAsrPq84PudrQb9K68IJleb1PYmLTXgwn6-CSGH3o1_NKklKAViheFj48Kafg5Yt7pTcilBr2JOIxZU6koV4pLWdAPL9D1MKZY_B0oPuGKSPqPWpkedYjdUC52B1E9lZzJiaCCFOryP1SZHjfBDRG7UPaPEpqHBJeGnBN2TyYJ6EMH6KMOKPz755V5ov_-N_sDBXWpfw</recordid><startdate>20230226</startdate><enddate>20230226</enddate><creator>Cheng, Hao</creator><creator>Li, Linnan</creator><creator>Xue, Junqiang</creator><creator>Ma, Jianying</creator><creator>Ge, Junbo</creator><general>MDPI AG</general><general>MDPI</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>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>COVID</scope><scope>DWQXO</scope><scope>FR3</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-1360-6290</orcidid></search><sort><creationdate>20230226</creationdate><title>TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner</title><author>Cheng, Hao ; Li, Linnan ; Xue, Junqiang ; Ma, Jianying ; Ge, Junbo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c483t-db8475f2bbc595ed5c1c18f59be591070444dbd04b19031fed7082b00d9aea0b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Acids</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biomarkers</topic><topic>Cardiac function</topic><topic>Cardiomyocytes</topic><topic>Congestive heart failure</topic><topic>Development and progression</topic><topic>Estrogens</topic><topic>Ethanol</topic><topic>Extracellular matrix</topic><topic>Extracellular Matrix - metabolism</topic><topic>Fibrosis</topic><topic>Genetic aspects</topic><topic>Glycoproteins</topic><topic>Health aspects</topic><topic>Heart attacks</topic><topic>Heart diseases</topic><topic>Heart failure</topic><topic>Heart Injuries - metabolism</topic><topic>Heart Injuries - pathology</topic><topic>Hypoxia</topic><topic>Hypoxia - complications</topic><topic>Hypoxia - metabolism</topic><topic>Laboratory animals</topic><topic>Messenger RNA</topic><topic>Methyltransferases</topic><topic>Methyltransferases - genetics</topic><topic>Methyltransferases - metabolism</topic><topic>Mice</topic><topic>mRNA stability</topic><topic>Myocardial infarction</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>N6-methyladenosine</topic><topic>Physiology</topic><topic>RNA modification</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Software</topic><topic>Tenascin</topic><topic>Tenascin - genetics</topic><topic>Tenascin C</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cheng, Hao</creatorcontrib><creatorcontrib>Li, Linnan</creatorcontrib><creatorcontrib>Xue, Junqiang</creatorcontrib><creatorcontrib>Ma, Jianying</creatorcontrib><creatorcontrib>Ge, Junbo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>Coronavirus Research Database</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest - Publicly Available Content 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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genes</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cheng, Hao</au><au>Li, Linnan</au><au>Xue, Junqiang</au><au>Ma, Jianying</au><au>Ge, Junbo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner</atitle><jtitle>Genes</jtitle><addtitle>Genes (Basel)</addtitle><date>2023-02-26</date><risdate>2023</risdate><volume>14</volume><issue>3</issue><spage>591</spage><pages>591-</pages><issn>2073-4425</issn><eissn>2073-4425</eissn><abstract>Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is also a key regulator of proliferation and apoptosis in cardiomyocytes. As a significant m
A regulator, METTL3 binds m
A sites in mRNA to control its degradation, maturation, stabilization, and translation. Whether METTL3 regulates the occurrence and development of myocardial infarction through the m
A modification of TNC mRNA deserves our study. Here, we have demonstrated that overexpression of METTL3 aggravated cardiac dysfunction and cardiac fibrosis after 4 weeks after MI. Moreover, we also demonstrated that TNC resulted in cardiac fibrosis and cardiomyocyte apoptosis after MI. Mechanistically, METTL3 led to enhanced m
A levels of TNC mRNA and promoted TNC mRNA stability. Then, we mutated one m
A site "A" to "T", and the binding ability of METTL3 was reduced. In conclusion, METTL3 is involved in cardiac fibrosis and cardiomyocyte apoptosis by increasing m
A levels of TNC mRNA and may be a promising target for the therapy of cardiac fibrosis after MI.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>36980863</pmid><doi>10.3390/genes14030591</doi><orcidid>https://orcid.org/0000-0003-1360-6290</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Acids Animals Apoptosis Biomarkers Cardiac function Cardiomyocytes Congestive heart failure Development and progression Estrogens Ethanol Extracellular matrix Extracellular Matrix - metabolism Fibrosis Genetic aspects Glycoproteins Health aspects Heart attacks Heart diseases Heart failure Heart Injuries - metabolism Heart Injuries - pathology Hypoxia Hypoxia - complications Hypoxia - metabolism Laboratory animals Messenger RNA Methyltransferases Methyltransferases - genetics Methyltransferases - metabolism Mice mRNA stability Myocardial infarction Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocytes, Cardiac - metabolism N6-methyladenosine Physiology RNA modification RNA, Messenger - genetics RNA, Messenger - metabolism Software Tenascin Tenascin - genetics Tenascin C |
| title | TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner |
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