Coordination of PRKCA/PRKCA-AS1 interplay facilitates DNA methyltransferase 1 recruitment on DNA methylation to affect protein kinase C alpha transcription in mitral valve of rheumatic heart disease
In the present study, mitral valve tissues from three mitral stenosis patients with RHD by valve replacement and two healthy donors were harvested and conducted DNA methylation signature on PRKCA by MeDIP-qPCR. The presence of hypomethylated CpG islands at promoter and 5ʹ terminal of PRKCA was obser...
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| Veröffentlicht in: | Bioengineered 2021-01, Vol.12 (1), p.5904-5915 |
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| creator | Xie, Zan Wang, Qianli Hu, Shaojuan |
| description | In the present study, mitral valve tissues from three mitral stenosis patients with RHD by valve replacement and two healthy donors were harvested and conducted DNA methylation signature on PRKCA by MeDIP-qPCR. The presence of hypomethylated CpG islands at promoter and 5ʹ terminal of PRKCA was observed in RHD accompanied with highly expressed PRKCA and down-regulated antisense long non-coding RNA (lncRNA) PRKCA-AS1 compared to health control. Furthermore, the enrichments of DNMT1/3A/3B on PRKCA were detected by ChIP-qPCR assay in vivo and in human cardiomyocyte AC16 and RL-14 cells exposed to TNF-α in vitro, and both demonstrated that DNMT1 substantially contributed to DNA methylation. Additionally, PRKCA-AS1 was further determined to bind with promoter of PRKCA via 5ʹ terminal and interact with DNMT1 via 3ʹ terminal. Taken together, our results illuminated a novel regulatory mechanism of DNA methylation on regulating PRKCA transcription through lncRNA PRKCA-AS1, and shed light on the molecular pathogenesis of RHD occurrence. |
| doi_str_mv | 10.1080/21655979.2021.1971482 |
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The presence of hypomethylated CpG islands at promoter and 5ʹ terminal of PRKCA was observed in RHD accompanied with highly expressed PRKCA and down-regulated antisense long non-coding RNA (lncRNA) PRKCA-AS1 compared to health control. Furthermore, the enrichments of DNMT1/3A/3B on PRKCA were detected by ChIP-qPCR assay in vivo and in human cardiomyocyte AC16 and RL-14 cells exposed to TNF-α in vitro, and both demonstrated that DNMT1 substantially contributed to DNA methylation. Additionally, PRKCA-AS1 was further determined to bind with promoter of PRKCA via 5ʹ terminal and interact with DNMT1 via 3ʹ terminal. Taken together, our results illuminated a novel regulatory mechanism of DNA methylation on regulating PRKCA transcription through lncRNA PRKCA-AS1, and shed light on the molecular pathogenesis of RHD occurrence.</description><identifier>ISSN: 2165-5979</identifier><identifier>EISSN: 2165-5987</identifier><identifier>DOI: 10.1080/21655979.2021.1971482</identifier><identifier>PMID: 34482802</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>Aged ; DNA (Cytosine-5-)-Methyltransferase 1 - genetics ; DNA (Cytosine-5-)-Methyltransferase 1 - metabolism ; dna methylation ; DNA Methylation - genetics ; dnmt1 ; Female ; Humans ; Male ; Middle Aged ; Mitral Valve - metabolism ; prkca-as1 ; Promoter Regions, Genetic - genetics ; protein kinase c alpha ; Protein Kinase C-alpha - genetics ; Protein Kinase C-alpha - metabolism ; Research Paper ; Rheumatic heart disease ; Rheumatic Heart Disease - genetics ; Rheumatic Heart Disease - metabolism ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism</subject><ispartof>Bioengineered, 2021-01, Vol.12 (1), p.5904-5915</ispartof><rights>2021 The Author(s). 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The presence of hypomethylated CpG islands at promoter and 5ʹ terminal of PRKCA was observed in RHD accompanied with highly expressed PRKCA and down-regulated antisense long non-coding RNA (lncRNA) PRKCA-AS1 compared to health control. Furthermore, the enrichments of DNMT1/3A/3B on PRKCA were detected by ChIP-qPCR assay in vivo and in human cardiomyocyte AC16 and RL-14 cells exposed to TNF-α in vitro, and both demonstrated that DNMT1 substantially contributed to DNA methylation. Additionally, PRKCA-AS1 was further determined to bind with promoter of PRKCA via 5ʹ terminal and interact with DNMT1 via 3ʹ terminal. Taken together, our results illuminated a novel regulatory mechanism of DNA methylation on regulating PRKCA transcription through lncRNA PRKCA-AS1, and shed light on the molecular pathogenesis of RHD occurrence.</description><subject>Aged</subject><subject>DNA (Cytosine-5-)-Methyltransferase 1 - genetics</subject><subject>DNA (Cytosine-5-)-Methyltransferase 1 - metabolism</subject><subject>dna methylation</subject><subject>DNA Methylation - genetics</subject><subject>dnmt1</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Mitral Valve - metabolism</subject><subject>prkca-as1</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>protein kinase c alpha</subject><subject>Protein Kinase C-alpha - genetics</subject><subject>Protein Kinase C-alpha - metabolism</subject><subject>Research Paper</subject><subject>Rheumatic heart disease</subject><subject>Rheumatic Heart Disease - genetics</subject><subject>Rheumatic Heart Disease - metabolism</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><issn>2165-5979</issn><issn>2165-5987</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>EIF</sourceid><recordid>eNp9kttu1DAQhiMEolXpI4B8yU22dhKfbhCr5VBEBYjDteU4NjE4cWo7i_YFea46u9sFbrixrX_--WasmaJ4iuAKQQavKkQw5pSvKlihFeIUNax6UJwveok5ow9Pb8rPissYf0AIEawbTNnj4qxusp_B6rz4vfE-dHaUyfoReAM-fX6_WV_tz3L9BQE7Jh0mJ3fASGWdTTLpCF59WINBp37nUpBjNDrIqAECQasw2zToMYHM-2M78JMH0hitEpiCT9qO4GcunTM3QLqpl2BPU8FOe3uODzZLDmyl2-qlvdDrecgwBXotQwKdjToDnhSPjHRRXx7vi-Lbm9dfN9flzce37zbrm1I1hKWyRpRWNSJ1qyrEcKc40ovEs9Jx1jRthyntOJEtVEhywjrVmbahtG5IQ0x9Ubw4cKe5HXSn8j9ze2IKdpBhJ7y04t_IaHvx3W8FY5AQhjPg-REQ_O2sYxKDjUo7J0ft5ygqTDhBGDKWrfhgVcHHGLQ5lUFQLGsg7tdALGsgjmuQ85793eMp637o2fDyYLCj8WGQv3xwnUhy53wweQDKRlH_v8YdcGvFjw</recordid><startdate>20210101</startdate><enddate>20210101</enddate><creator>Xie, Zan</creator><creator>Wang, Qianli</creator><creator>Hu, Shaojuan</creator><general>Taylor & Francis</general><scope>0YH</scope><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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20210101</creationdate><title>Coordination of PRKCA/PRKCA-AS1 interplay facilitates DNA methyltransferase 1 recruitment on DNA methylation to affect protein kinase C alpha transcription in mitral valve of rheumatic heart disease</title><author>Xie, Zan ; Wang, Qianli ; Hu, Shaojuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-317723163bc2185dc91e1772963bd9844bd577d96ab0c1a968dcdfb47734646f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Aged</topic><topic>DNA (Cytosine-5-)-Methyltransferase 1 - genetics</topic><topic>DNA (Cytosine-5-)-Methyltransferase 1 - metabolism</topic><topic>dna methylation</topic><topic>DNA Methylation - genetics</topic><topic>dnmt1</topic><topic>Female</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Mitral Valve - metabolism</topic><topic>prkca-as1</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>protein kinase c alpha</topic><topic>Protein Kinase C-alpha - genetics</topic><topic>Protein Kinase C-alpha - metabolism</topic><topic>Research Paper</topic><topic>Rheumatic heart disease</topic><topic>Rheumatic Heart Disease - genetics</topic><topic>Rheumatic Heart Disease - metabolism</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xie, Zan</creatorcontrib><creatorcontrib>Wang, Qianli</creatorcontrib><creatorcontrib>Hu, Shaojuan</creatorcontrib><collection>Access via Taylor & Francis (Open Access Collection)</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Bioengineered</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xie, Zan</au><au>Wang, Qianli</au><au>Hu, Shaojuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Coordination of PRKCA/PRKCA-AS1 interplay facilitates DNA methyltransferase 1 recruitment on DNA methylation to affect protein kinase C alpha transcription in mitral valve of rheumatic heart disease</atitle><jtitle>Bioengineered</jtitle><addtitle>Bioengineered</addtitle><date>2021-01-01</date><risdate>2021</risdate><volume>12</volume><issue>1</issue><spage>5904</spage><epage>5915</epage><pages>5904-5915</pages><issn>2165-5979</issn><eissn>2165-5987</eissn><abstract>In the present study, mitral valve tissues from three mitral stenosis patients with RHD by valve replacement and two healthy donors were harvested and conducted DNA methylation signature on PRKCA by MeDIP-qPCR. The presence of hypomethylated CpG islands at promoter and 5ʹ terminal of PRKCA was observed in RHD accompanied with highly expressed PRKCA and down-regulated antisense long non-coding RNA (lncRNA) PRKCA-AS1 compared to health control. Furthermore, the enrichments of DNMT1/3A/3B on PRKCA were detected by ChIP-qPCR assay in vivo and in human cardiomyocyte AC16 and RL-14 cells exposed to TNF-α in vitro, and both demonstrated that DNMT1 substantially contributed to DNA methylation. Additionally, PRKCA-AS1 was further determined to bind with promoter of PRKCA via 5ʹ terminal and interact with DNMT1 via 3ʹ terminal. Taken together, our results illuminated a novel regulatory mechanism of DNA methylation on regulating PRKCA transcription through lncRNA PRKCA-AS1, and shed light on the molecular pathogenesis of RHD occurrence.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>34482802</pmid><doi>10.1080/21655979.2021.1971482</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged DNA (Cytosine-5-)-Methyltransferase 1 - genetics DNA (Cytosine-5-)-Methyltransferase 1 - metabolism dna methylation DNA Methylation - genetics dnmt1 Female Humans Male Middle Aged Mitral Valve - metabolism prkca-as1 Promoter Regions, Genetic - genetics protein kinase c alpha Protein Kinase C-alpha - genetics Protein Kinase C-alpha - metabolism Research Paper Rheumatic heart disease Rheumatic Heart Disease - genetics Rheumatic Heart Disease - metabolism RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism |
| title | Coordination of PRKCA/PRKCA-AS1 interplay facilitates DNA methyltransferase 1 recruitment on DNA methylation to affect protein kinase C alpha transcription in mitral valve of rheumatic heart disease |
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