Antihypertrophic Memory After Regression of Exercise-Induced Physiological Myocardial Hypertrophy Is Mediated by the Long Noncoding RNA Mhrt779
Exercise can induce physiological myocardial hypertrophy (PMH), and former athletes can live 5 to 6 years longer than nonathletic controls, suggesting a benefit after regression of PMH. We previously reported that regression of pathological myocardial hypertrophy has antihypertrophic effects. Accord...
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| creator | Lin, Hairuo Zhu, Yingqi Zheng, Cankun Hu, Donghong Ma, Siyuan Chen, Lin Wang, Qiancheng Chen, Zhenhuan Xie, Jiahe Yan, Yi Huang, Xiaobo Liao, Wangjun Kitakaze, Masafumi Bin, Jianping Liao, Yulin |
| description | Exercise can induce physiological myocardial hypertrophy (PMH), and former athletes can live 5 to 6 years longer than nonathletic controls, suggesting a benefit after regression of PMH. We previously reported that regression of pathological myocardial hypertrophy has antihypertrophic effects. Accordingly, we hypothesized that antihypertrophic memory exists even after PMH has regressed, increasing myocardial resistance to subsequent pathological hypertrophic stress.
C57BL/6 mice were submitted to 21 days of swimming training to develop PMH. After termination of exercise, PMH regressed within 1 week. PMH regression mice (exercise hypertrophic preconditioning [EHP] group) and sedentary mice (control group) then underwent transverse aortic constriction or a sham operation for 4 weeks. Cardiac remodeling and function were evaluated with echocardiography, invasive left ventricular hemodynamic measurement, and histological analysis. LncRNA sequencing, chromatin immunoprecipitation assay, and comprehensive identification of RNA-binding proteins by mass spectrometry and Western blot were used to investigate the role of
involved in the antihypertrophic effect induced by EHP.
At 1 and 4 weeks after transverse aortic constriction, the EHP group showed less increase in myocardial hypertrophy and lower expression of the
and
genes than the sedentary group. At 4 weeks after transverse aortic constriction, EHP mice had less pulmonary congestion, smaller left ventricular dimensions and end-diastolic pressure, and a larger left ventricular ejection fraction and maximum pressure change rate than sedentary mice. Quantitative polymerase chain reaction revealed that the long noncoding myosin heavy chain-associated RNA transcript
was one of the markedly upregulated lncRNAs in the EHP group. Silencing of
attenuated the antihypertrophic effect of EHP in mice with transverse aortic constriction and in cultured cardiomyocytes treated with angiotensin II, and overexpression enhanced the antihypertrophic effect. Using chromatin immunoprecipitation assay and quantitative polymerase chain reaction, we found that EHP increased histone 3 trimethylation (H3K4me3 and H3K36me3) at the a4 promoter of
. Comprehensive identification of RNA-binding proteins by mass spectrometry and Western blot showed that
can bind SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 (Brg1) to inhibit the activation of the histone deacetylase 2 (Hdac2)/phosphorylated s |
| doi_str_mv | 10.1161/CIRCULATIONAHA.120.047000 |
| format | Article |
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C57BL/6 mice were submitted to 21 days of swimming training to develop PMH. After termination of exercise, PMH regressed within 1 week. PMH regression mice (exercise hypertrophic preconditioning [EHP] group) and sedentary mice (control group) then underwent transverse aortic constriction or a sham operation for 4 weeks. Cardiac remodeling and function were evaluated with echocardiography, invasive left ventricular hemodynamic measurement, and histological analysis. LncRNA sequencing, chromatin immunoprecipitation assay, and comprehensive identification of RNA-binding proteins by mass spectrometry and Western blot were used to investigate the role of
involved in the antihypertrophic effect induced by EHP.
At 1 and 4 weeks after transverse aortic constriction, the EHP group showed less increase in myocardial hypertrophy and lower expression of the
and
genes than the sedentary group. At 4 weeks after transverse aortic constriction, EHP mice had less pulmonary congestion, smaller left ventricular dimensions and end-diastolic pressure, and a larger left ventricular ejection fraction and maximum pressure change rate than sedentary mice. Quantitative polymerase chain reaction revealed that the long noncoding myosin heavy chain-associated RNA transcript
was one of the markedly upregulated lncRNAs in the EHP group. Silencing of
attenuated the antihypertrophic effect of EHP in mice with transverse aortic constriction and in cultured cardiomyocytes treated with angiotensin II, and overexpression enhanced the antihypertrophic effect. Using chromatin immunoprecipitation assay and quantitative polymerase chain reaction, we found that EHP increased histone 3 trimethylation (H3K4me3 and H3K36me3) at the a4 promoter of
. Comprehensive identification of RNA-binding proteins by mass spectrometry and Western blot showed that
can bind SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 (Brg1) to inhibit the activation of the histone deacetylase 2 (Hdac2)/phosphorylated serine/threonine kinase (Akt)/phosphorylated glycogen synthase kinase 3β(p-GSK3β) pathway induced by pressure overload.
Myocardial hypertrophy preconditioning evoked by exercise increases resistance to pathological stress via an antihypertrophic effect mediated by a signal pathway of
/Brg1/Hdac2/p-Akt/p-GSK3β.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/CIRCULATIONAHA.120.047000</identifier><identifier>PMID: 33757294</identifier><language>eng</language><publisher>United States: Lippincott Williams & Wilkins</publisher><subject>Animals ; Atrial Natriuretic Factor - genetics ; Atrial Natriuretic Factor - metabolism ; Cardiomegaly - genetics ; Cardiomegaly - therapy ; Disease Models, Animal ; Echocardiography ; Glycogen Synthase Kinase 3 beta - metabolism ; Hemodynamics ; Histone Deacetylase 2 - metabolism ; Mice ; Mice, Inbred C57BL ; Original s ; Physical Conditioning, Animal ; Proto-Oncogene Proteins c-akt - metabolism ; RNA Interference ; RNA, Long Noncoding - antagonists & inhibitors ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; RNA, Small Interfering - metabolism ; Signal Transduction ; Up-Regulation ; Ventricular Function, Left - physiology ; Ventricular Remodeling</subject><ispartof>Circulation (New York, N.Y.), 2021-06, Vol.143 (23), p.2277-2292</ispartof><rights>Lippincott Williams & Wilkins</rights><rights>2021 The Authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5249-628f72e70caa8b44e7567af7614e1131f13e929365929ae311a3f372928332603</citedby><cites>FETCH-LOGICAL-c5249-628f72e70caa8b44e7567af7614e1131f13e929365929ae311a3f372928332603</cites><orcidid>0000-0001-5961-390X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3673,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33757294$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Hairuo</creatorcontrib><creatorcontrib>Zhu, Yingqi</creatorcontrib><creatorcontrib>Zheng, Cankun</creatorcontrib><creatorcontrib>Hu, Donghong</creatorcontrib><creatorcontrib>Ma, Siyuan</creatorcontrib><creatorcontrib>Chen, Lin</creatorcontrib><creatorcontrib>Wang, Qiancheng</creatorcontrib><creatorcontrib>Chen, Zhenhuan</creatorcontrib><creatorcontrib>Xie, Jiahe</creatorcontrib><creatorcontrib>Yan, Yi</creatorcontrib><creatorcontrib>Huang, Xiaobo</creatorcontrib><creatorcontrib>Liao, Wangjun</creatorcontrib><creatorcontrib>Kitakaze, Masafumi</creatorcontrib><creatorcontrib>Bin, Jianping</creatorcontrib><creatorcontrib>Liao, Yulin</creatorcontrib><title>Antihypertrophic Memory After Regression of Exercise-Induced Physiological Myocardial Hypertrophy Is Mediated by the Long Noncoding RNA Mhrt779</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Exercise can induce physiological myocardial hypertrophy (PMH), and former athletes can live 5 to 6 years longer than nonathletic controls, suggesting a benefit after regression of PMH. We previously reported that regression of pathological myocardial hypertrophy has antihypertrophic effects. Accordingly, we hypothesized that antihypertrophic memory exists even after PMH has regressed, increasing myocardial resistance to subsequent pathological hypertrophic stress.
C57BL/6 mice were submitted to 21 days of swimming training to develop PMH. After termination of exercise, PMH regressed within 1 week. PMH regression mice (exercise hypertrophic preconditioning [EHP] group) and sedentary mice (control group) then underwent transverse aortic constriction or a sham operation for 4 weeks. Cardiac remodeling and function were evaluated with echocardiography, invasive left ventricular hemodynamic measurement, and histological analysis. LncRNA sequencing, chromatin immunoprecipitation assay, and comprehensive identification of RNA-binding proteins by mass spectrometry and Western blot were used to investigate the role of
involved in the antihypertrophic effect induced by EHP.
At 1 and 4 weeks after transverse aortic constriction, the EHP group showed less increase in myocardial hypertrophy and lower expression of the
and
genes than the sedentary group. At 4 weeks after transverse aortic constriction, EHP mice had less pulmonary congestion, smaller left ventricular dimensions and end-diastolic pressure, and a larger left ventricular ejection fraction and maximum pressure change rate than sedentary mice. Quantitative polymerase chain reaction revealed that the long noncoding myosin heavy chain-associated RNA transcript
was one of the markedly upregulated lncRNAs in the EHP group. Silencing of
attenuated the antihypertrophic effect of EHP in mice with transverse aortic constriction and in cultured cardiomyocytes treated with angiotensin II, and overexpression enhanced the antihypertrophic effect. Using chromatin immunoprecipitation assay and quantitative polymerase chain reaction, we found that EHP increased histone 3 trimethylation (H3K4me3 and H3K36me3) at the a4 promoter of
. Comprehensive identification of RNA-binding proteins by mass spectrometry and Western blot showed that
can bind SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 (Brg1) to inhibit the activation of the histone deacetylase 2 (Hdac2)/phosphorylated serine/threonine kinase (Akt)/phosphorylated glycogen synthase kinase 3β(p-GSK3β) pathway induced by pressure overload.
Myocardial hypertrophy preconditioning evoked by exercise increases resistance to pathological stress via an antihypertrophic effect mediated by a signal pathway of
/Brg1/Hdac2/p-Akt/p-GSK3β.</description><subject>Animals</subject><subject>Atrial Natriuretic Factor - genetics</subject><subject>Atrial Natriuretic Factor - metabolism</subject><subject>Cardiomegaly - genetics</subject><subject>Cardiomegaly - therapy</subject><subject>Disease Models, Animal</subject><subject>Echocardiography</subject><subject>Glycogen Synthase Kinase 3 beta - metabolism</subject><subject>Hemodynamics</subject><subject>Histone Deacetylase 2 - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Original s</subject><subject>Physical Conditioning, Animal</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>RNA Interference</subject><subject>RNA, Long Noncoding - antagonists & inhibitors</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Signal Transduction</subject><subject>Up-Regulation</subject><subject>Ventricular Function, Left - physiology</subject><subject>Ventricular Remodeling</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc-O0zAQxiMEYrsLr4DMjUuK_yWOL0hRtdBIbRdVu2fLdSaNIY2LnbDkKfaVcdWlYi-e8cw3nz36JclHgueE5OTzotouHlblfXW3KZflnFA8x1xgjF8lM5JRnvKMydfJLFZkKhilV8l1CD_iNWcie5tcsRgElXyWPJX9YNvpCH7w7thag9ZwcH5CZTOAR1vYewjBuh65Bt3-AW9sgLTq69FAjb63U-x1bm-N7tB6ckb72sZ0eXGcUBWiZ6wOcWA3oaEFtHL9Hm1cb1xtY7bdlGjd-kEI-S550-guwPvneJM8fL29XyzT1d23alGuUhP3k2lOi0ZQENhoXew4B5HlQjciJxwIYaQhDCSVLM_iqYERolnD4sq0YIzmmN0kX86-x3F3gNpAP3jdqaO3B-0n5bRVLzu9bdXe_VYFEYJLHg0-PRt492uEMKiDDQa6TvfgxqBoFpHEhUQRpfIsNd6F4KG5PEOwOgFVL4GqCFSdgcbZD___8zL5j2AU8LPg0XWRWPjZjY_gVQu6G1qFTx6YiJRiSnCOC5yeSpL9BVJtrys</recordid><startdate>20210608</startdate><enddate>20210608</enddate><creator>Lin, Hairuo</creator><creator>Zhu, Yingqi</creator><creator>Zheng, Cankun</creator><creator>Hu, Donghong</creator><creator>Ma, Siyuan</creator><creator>Chen, Lin</creator><creator>Wang, Qiancheng</creator><creator>Chen, Zhenhuan</creator><creator>Xie, Jiahe</creator><creator>Yan, Yi</creator><creator>Huang, Xiaobo</creator><creator>Liao, Wangjun</creator><creator>Kitakaze, Masafumi</creator><creator>Bin, Jianping</creator><creator>Liao, Yulin</creator><general>Lippincott Williams & Wilkins</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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-5961-390X</orcidid></search><sort><creationdate>20210608</creationdate><title>Antihypertrophic Memory After Regression of Exercise-Induced Physiological Myocardial Hypertrophy Is Mediated by the Long Noncoding RNA Mhrt779</title><author>Lin, Hairuo ; Zhu, Yingqi ; Zheng, Cankun ; Hu, Donghong ; Ma, Siyuan ; Chen, Lin ; Wang, Qiancheng ; Chen, Zhenhuan ; Xie, Jiahe ; Yan, Yi ; Huang, Xiaobo ; Liao, Wangjun ; Kitakaze, Masafumi ; Bin, Jianping ; Liao, Yulin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5249-628f72e70caa8b44e7567af7614e1131f13e929365929ae311a3f372928332603</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Atrial Natriuretic Factor - genetics</topic><topic>Atrial Natriuretic Factor - metabolism</topic><topic>Cardiomegaly - genetics</topic><topic>Cardiomegaly - therapy</topic><topic>Disease Models, Animal</topic><topic>Echocardiography</topic><topic>Glycogen Synthase Kinase 3 beta - metabolism</topic><topic>Hemodynamics</topic><topic>Histone Deacetylase 2 - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Original s</topic><topic>Physical Conditioning, Animal</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>RNA Interference</topic><topic>RNA, Long Noncoding - antagonists & inhibitors</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Signal Transduction</topic><topic>Up-Regulation</topic><topic>Ventricular Function, Left - physiology</topic><topic>Ventricular Remodeling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, Hairuo</creatorcontrib><creatorcontrib>Zhu, Yingqi</creatorcontrib><creatorcontrib>Zheng, Cankun</creatorcontrib><creatorcontrib>Hu, Donghong</creatorcontrib><creatorcontrib>Ma, Siyuan</creatorcontrib><creatorcontrib>Chen, Lin</creatorcontrib><creatorcontrib>Wang, Qiancheng</creatorcontrib><creatorcontrib>Chen, Zhenhuan</creatorcontrib><creatorcontrib>Xie, Jiahe</creatorcontrib><creatorcontrib>Yan, Yi</creatorcontrib><creatorcontrib>Huang, Xiaobo</creatorcontrib><creatorcontrib>Liao, Wangjun</creatorcontrib><creatorcontrib>Kitakaze, Masafumi</creatorcontrib><creatorcontrib>Bin, Jianping</creatorcontrib><creatorcontrib>Liao, Yulin</creatorcontrib><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>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Hairuo</au><au>Zhu, Yingqi</au><au>Zheng, Cankun</au><au>Hu, Donghong</au><au>Ma, Siyuan</au><au>Chen, Lin</au><au>Wang, Qiancheng</au><au>Chen, Zhenhuan</au><au>Xie, Jiahe</au><au>Yan, Yi</au><au>Huang, Xiaobo</au><au>Liao, Wangjun</au><au>Kitakaze, Masafumi</au><au>Bin, Jianping</au><au>Liao, Yulin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antihypertrophic Memory After Regression of Exercise-Induced Physiological Myocardial Hypertrophy Is Mediated by the Long Noncoding RNA Mhrt779</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2021-06-08</date><risdate>2021</risdate><volume>143</volume><issue>23</issue><spage>2277</spage><epage>2292</epage><pages>2277-2292</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><abstract>Exercise can induce physiological myocardial hypertrophy (PMH), and former athletes can live 5 to 6 years longer than nonathletic controls, suggesting a benefit after regression of PMH. We previously reported that regression of pathological myocardial hypertrophy has antihypertrophic effects. Accordingly, we hypothesized that antihypertrophic memory exists even after PMH has regressed, increasing myocardial resistance to subsequent pathological hypertrophic stress.
C57BL/6 mice were submitted to 21 days of swimming training to develop PMH. After termination of exercise, PMH regressed within 1 week. PMH regression mice (exercise hypertrophic preconditioning [EHP] group) and sedentary mice (control group) then underwent transverse aortic constriction or a sham operation for 4 weeks. Cardiac remodeling and function were evaluated with echocardiography, invasive left ventricular hemodynamic measurement, and histological analysis. LncRNA sequencing, chromatin immunoprecipitation assay, and comprehensive identification of RNA-binding proteins by mass spectrometry and Western blot were used to investigate the role of
involved in the antihypertrophic effect induced by EHP.
At 1 and 4 weeks after transverse aortic constriction, the EHP group showed less increase in myocardial hypertrophy and lower expression of the
and
genes than the sedentary group. At 4 weeks after transverse aortic constriction, EHP mice had less pulmonary congestion, smaller left ventricular dimensions and end-diastolic pressure, and a larger left ventricular ejection fraction and maximum pressure change rate than sedentary mice. Quantitative polymerase chain reaction revealed that the long noncoding myosin heavy chain-associated RNA transcript
was one of the markedly upregulated lncRNAs in the EHP group. Silencing of
attenuated the antihypertrophic effect of EHP in mice with transverse aortic constriction and in cultured cardiomyocytes treated with angiotensin II, and overexpression enhanced the antihypertrophic effect. Using chromatin immunoprecipitation assay and quantitative polymerase chain reaction, we found that EHP increased histone 3 trimethylation (H3K4me3 and H3K36me3) at the a4 promoter of
. Comprehensive identification of RNA-binding proteins by mass spectrometry and Western blot showed that
can bind SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 (Brg1) to inhibit the activation of the histone deacetylase 2 (Hdac2)/phosphorylated serine/threonine kinase (Akt)/phosphorylated glycogen synthase kinase 3β(p-GSK3β) pathway induced by pressure overload.
Myocardial hypertrophy preconditioning evoked by exercise increases resistance to pathological stress via an antihypertrophic effect mediated by a signal pathway of
/Brg1/Hdac2/p-Akt/p-GSK3β.</abstract><cop>United States</cop><pub>Lippincott Williams & Wilkins</pub><pmid>33757294</pmid><doi>10.1161/CIRCULATIONAHA.120.047000</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0001-5961-390X</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 2021-06, Vol.143 (23), p.2277-2292 |
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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Atrial Natriuretic Factor - genetics Atrial Natriuretic Factor - metabolism Cardiomegaly - genetics Cardiomegaly - therapy Disease Models, Animal Echocardiography Glycogen Synthase Kinase 3 beta - metabolism Hemodynamics Histone Deacetylase 2 - metabolism Mice Mice, Inbred C57BL Original s Physical Conditioning, Animal Proto-Oncogene Proteins c-akt - metabolism RNA Interference RNA, Long Noncoding - antagonists & inhibitors RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism RNA, Small Interfering - metabolism Signal Transduction Up-Regulation Ventricular Function, Left - physiology Ventricular Remodeling |
| title | Antihypertrophic Memory After Regression of Exercise-Induced Physiological Myocardial Hypertrophy Is Mediated by the Long Noncoding RNA Mhrt779 |
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