Involvement of Reductive Stress in the Cardiomyopathy in Transgenic Mice With Cardiac-Specific Overexpression of Heat Shock Protein 27
Oxidative stress plays an important role in cardiac diseases, which has been well demonstrated, whereas the role of reductive stress has been poorly investigated. We and others have shown previously that heat shock protein 27 (Hsp27) plays a role as an antioxidant. To investigate whether overexpress...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2010-06, Vol.55 (6), p.1412-1417 |
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| container_title | Hypertension (Dallas, Tex. 1979) |
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| creator | Zhang, Xia Min, Xiaoyan Li, Chuanfu Benjamin, Ivor J Qian, Bo Zhang, Xiaojin Ding, Zhengnian Gao, Xiang Yao, Yuzhen Ma, Yujie Cheng, Yunling Liu, Li |
| description | Oxidative stress plays an important role in cardiac diseases, which has been well demonstrated, whereas the role of reductive stress has been poorly investigated. We and others have shown previously that heat shock protein 27 (Hsp27) plays a role as an antioxidant. To investigate whether overexpression of Hsp27 could lead to reductive stress and result in cardiomyopathy, we generated transgenic mice with different expression levels of Hsp27. We observed that transgenic mice with high levels of Hsp27 developed cardiomyopathy. The myopathic hearts were under reductive stress, which was evidenced by an increased ratio of reduced glutathione/oxidized glutathione and a decreased level of reactive oxygen species. In addition, upregulated glutathione peroxidase 1 and decreased iron content were revealed in the myopathic hearts. More importantly, inhibition of glutathione peroxidase 1 significantly attenuated the development of cardiomyopathy. The data indicate that the Hsp27-induced cardiomyopathy could be attributed to, at least in part, upregulation of glutathione peroxidase 1. Our findings suggest that reductive stress plays an important role in the development of cardiomyopathy and that Hsp27 may serve as a potential target for the treatment of patients with cardiomyopathy. |
| doi_str_mv | 10.1161/HYPERTENSIONAHA.109.147066 |
| format | Article |
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We and others have shown previously that heat shock protein 27 (Hsp27) plays a role as an antioxidant. To investigate whether overexpression of Hsp27 could lead to reductive stress and result in cardiomyopathy, we generated transgenic mice with different expression levels of Hsp27. We observed that transgenic mice with high levels of Hsp27 developed cardiomyopathy. The myopathic hearts were under reductive stress, which was evidenced by an increased ratio of reduced glutathione/oxidized glutathione and a decreased level of reactive oxygen species. In addition, upregulated glutathione peroxidase 1 and decreased iron content were revealed in the myopathic hearts. More importantly, inhibition of glutathione peroxidase 1 significantly attenuated the development of cardiomyopathy. The data indicate that the Hsp27-induced cardiomyopathy could be attributed to, at least in part, upregulation of glutathione peroxidase 1. Our findings suggest that reductive stress plays an important role in the development of cardiomyopathy and that Hsp27 may serve as a potential target for the treatment of patients with cardiomyopathy.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/HYPERTENSIONAHA.109.147066</identifier><identifier>PMID: 20439823</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Analysis of Variance ; Animals ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Biomarkers - metabolism ; Blood and lymphatic vessels ; Blood Pressure Determination ; Cardiology. Vascular system ; Cardiomyopathy, Hypertrophic - diagnostic imaging ; Cardiomyopathy, Hypertrophic - metabolism ; Cardiomyopathy, Hypertrophic - physiopathology ; Disease Models, Animal ; Echocardiography ; Female ; Ferritins - metabolism ; Gene Expression Regulation ; Glutathione Peroxidase - genetics ; Glutathione Peroxidase - metabolism ; Heart ; Heart Function Tests ; HSP27 Heat-Shock Proteins - genetics ; HSP27 Heat-Shock Proteins - metabolism ; Immunohistochemistry ; Male ; Medical sciences ; Mice ; Mice, Transgenic ; Myocarditis. Cardiomyopathies ; Myocytes, Cardiac - pathology ; Myocytes, Cardiac - ultrastructure ; Oxidative Stress - physiology ; Random Allocation ; Reference Values ; Up-Regulation</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2010-06, Vol.55 (6), p.1412-1417</ispartof><rights>2010 American Heart Association, Inc.</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5023-e6ab87b013c47e886c8e4629d380bb096cb594e541fe664f4b0fef98fc33cda33</citedby><cites>FETCH-LOGICAL-c5023-e6ab87b013c47e886c8e4629d380bb096cb594e541fe664f4b0fef98fc33cda33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22853921$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20439823$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Xia</creatorcontrib><creatorcontrib>Min, Xiaoyan</creatorcontrib><creatorcontrib>Li, Chuanfu</creatorcontrib><creatorcontrib>Benjamin, Ivor J</creatorcontrib><creatorcontrib>Qian, Bo</creatorcontrib><creatorcontrib>Zhang, Xiaojin</creatorcontrib><creatorcontrib>Ding, Zhengnian</creatorcontrib><creatorcontrib>Gao, Xiang</creatorcontrib><creatorcontrib>Yao, Yuzhen</creatorcontrib><creatorcontrib>Ma, Yujie</creatorcontrib><creatorcontrib>Cheng, Yunling</creatorcontrib><creatorcontrib>Liu, Li</creatorcontrib><title>Involvement of Reductive Stress in the Cardiomyopathy in Transgenic Mice With Cardiac-Specific Overexpression of Heat Shock Protein 27</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>Oxidative stress plays an important role in cardiac diseases, which has been well demonstrated, whereas the role of reductive stress has been poorly investigated. We and others have shown previously that heat shock protein 27 (Hsp27) plays a role as an antioxidant. To investigate whether overexpression of Hsp27 could lead to reductive stress and result in cardiomyopathy, we generated transgenic mice with different expression levels of Hsp27. We observed that transgenic mice with high levels of Hsp27 developed cardiomyopathy. The myopathic hearts were under reductive stress, which was evidenced by an increased ratio of reduced glutathione/oxidized glutathione and a decreased level of reactive oxygen species. In addition, upregulated glutathione peroxidase 1 and decreased iron content were revealed in the myopathic hearts. More importantly, inhibition of glutathione peroxidase 1 significantly attenuated the development of cardiomyopathy. The data indicate that the Hsp27-induced cardiomyopathy could be attributed to, at least in part, upregulation of glutathione peroxidase 1. Our findings suggest that reductive stress plays an important role in the development of cardiomyopathy and that Hsp27 may serve as a potential target for the treatment of patients with cardiomyopathy.</description><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - metabolism</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure Determination</subject><subject>Cardiology. Vascular system</subject><subject>Cardiomyopathy, Hypertrophic - diagnostic imaging</subject><subject>Cardiomyopathy, Hypertrophic - metabolism</subject><subject>Cardiomyopathy, Hypertrophic - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Echocardiography</subject><subject>Female</subject><subject>Ferritins - metabolism</subject><subject>Gene Expression Regulation</subject><subject>Glutathione Peroxidase - genetics</subject><subject>Glutathione Peroxidase - metabolism</subject><subject>Heart</subject><subject>Heart Function Tests</subject><subject>HSP27 Heat-Shock Proteins - genetics</subject><subject>HSP27 Heat-Shock Proteins - metabolism</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Myocarditis. Cardiomyopathies</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Myocytes, Cardiac - ultrastructure</subject><subject>Oxidative Stress - physiology</subject><subject>Random Allocation</subject><subject>Reference Values</subject><subject>Up-Regulation</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkd2O0zAQhSMEYrsLr4AsJMRViv_iJNxVVaGVlu1qWwRcRY4zIWaTONhOd_sCPDeuUkBiJMvy-Jsz0jlR9JrgOSGCvFt_u13d7Vc3u832ZrFezAnO54SnWIgn0YwklMc8EexpNMMk53FOyNeL6NK5HxgTznn6PLqgmLM8o2wW_dr0B9MeoIPeI1OjO6hG5fUB0M5bcA7pHvkG0FLaSpvuaAbpm-Opu7eyd9-h1wp90grQF-2bCZMq3g2gdB2-tgew8DicpLTpTxvWID3aNUbdo1trPAQpmr6IntWydfDyfF9Fnz-s9st1fL39uFkurmOVYMpiELLM0hITpngKWSZUBlzQvGIZLkucC1UmOYeEkxqE4DUvcQ11ntWKMVVJxq6it5PuYM3PEZwvOu0UtK3swYyuSFmoNHgYyPcTqaxxzkJdDFZ30h4LgotTDMV_MYR-XkwxhOFX5zVj2UH1d_SP7wF4cwakU7Ktg5dKu38czRKWUxI4PnEPpvVg3X07PoAtGpCtbwocilORxRQTjEV4xeEE-d_xUaPM</recordid><startdate>201006</startdate><enddate>201006</enddate><creator>Zhang, Xia</creator><creator>Min, Xiaoyan</creator><creator>Li, Chuanfu</creator><creator>Benjamin, Ivor J</creator><creator>Qian, Bo</creator><creator>Zhang, Xiaojin</creator><creator>Ding, Zhengnian</creator><creator>Gao, Xiang</creator><creator>Yao, Yuzhen</creator><creator>Ma, Yujie</creator><creator>Cheng, Yunling</creator><creator>Liu, Li</creator><general>American Heart Association, Inc</general><general>Lippincott Williams & Wilkins</general><scope>IQODW</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></search><sort><creationdate>201006</creationdate><title>Involvement of Reductive Stress in the Cardiomyopathy in Transgenic Mice With Cardiac-Specific Overexpression of Heat Shock Protein 27</title><author>Zhang, Xia ; Min, Xiaoyan ; Li, Chuanfu ; Benjamin, Ivor J ; Qian, Bo ; Zhang, Xiaojin ; Ding, Zhengnian ; Gao, Xiang ; Yao, Yuzhen ; Ma, Yujie ; Cheng, Yunling ; Liu, Li</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5023-e6ab87b013c47e886c8e4629d380bb096cb594e541fe664f4b0fef98fc33cda33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - metabolism</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure Determination</topic><topic>Cardiology. Vascular system</topic><topic>Cardiomyopathy, Hypertrophic - diagnostic imaging</topic><topic>Cardiomyopathy, Hypertrophic - metabolism</topic><topic>Cardiomyopathy, Hypertrophic - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Echocardiography</topic><topic>Female</topic><topic>Ferritins - metabolism</topic><topic>Gene Expression Regulation</topic><topic>Glutathione Peroxidase - genetics</topic><topic>Glutathione Peroxidase - metabolism</topic><topic>Heart</topic><topic>Heart Function Tests</topic><topic>HSP27 Heat-Shock Proteins - genetics</topic><topic>HSP27 Heat-Shock Proteins - metabolism</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Myocarditis. Cardiomyopathies</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Myocytes, Cardiac - ultrastructure</topic><topic>Oxidative Stress - physiology</topic><topic>Random Allocation</topic><topic>Reference Values</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Xia</creatorcontrib><creatorcontrib>Min, Xiaoyan</creatorcontrib><creatorcontrib>Li, Chuanfu</creatorcontrib><creatorcontrib>Benjamin, Ivor J</creatorcontrib><creatorcontrib>Qian, Bo</creatorcontrib><creatorcontrib>Zhang, Xiaojin</creatorcontrib><creatorcontrib>Ding, Zhengnian</creatorcontrib><creatorcontrib>Gao, Xiang</creatorcontrib><creatorcontrib>Yao, Yuzhen</creatorcontrib><creatorcontrib>Ma, Yujie</creatorcontrib><creatorcontrib>Cheng, Yunling</creatorcontrib><creatorcontrib>Liu, Li</creatorcontrib><collection>Pascal-Francis</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><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Xia</au><au>Min, Xiaoyan</au><au>Li, Chuanfu</au><au>Benjamin, Ivor J</au><au>Qian, Bo</au><au>Zhang, Xiaojin</au><au>Ding, Zhengnian</au><au>Gao, Xiang</au><au>Yao, Yuzhen</au><au>Ma, Yujie</au><au>Cheng, Yunling</au><au>Liu, Li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of Reductive Stress in the Cardiomyopathy in Transgenic Mice With Cardiac-Specific Overexpression of Heat Shock Protein 27</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2010-06</date><risdate>2010</risdate><volume>55</volume><issue>6</issue><spage>1412</spage><epage>1417</epage><pages>1412-1417</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>Oxidative stress plays an important role in cardiac diseases, which has been well demonstrated, whereas the role of reductive stress has been poorly investigated. We and others have shown previously that heat shock protein 27 (Hsp27) plays a role as an antioxidant. To investigate whether overexpression of Hsp27 could lead to reductive stress and result in cardiomyopathy, we generated transgenic mice with different expression levels of Hsp27. We observed that transgenic mice with high levels of Hsp27 developed cardiomyopathy. The myopathic hearts were under reductive stress, which was evidenced by an increased ratio of reduced glutathione/oxidized glutathione and a decreased level of reactive oxygen species. In addition, upregulated glutathione peroxidase 1 and decreased iron content were revealed in the myopathic hearts. More importantly, inhibition of glutathione peroxidase 1 significantly attenuated the development of cardiomyopathy. The data indicate that the Hsp27-induced cardiomyopathy could be attributed to, at least in part, upregulation of glutathione peroxidase 1. Our findings suggest that reductive stress plays an important role in the development of cardiomyopathy and that Hsp27 may serve as a potential target for the treatment of patients with cardiomyopathy.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>20439823</pmid><doi>10.1161/HYPERTENSIONAHA.109.147066</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0194-911X |
| ispartof | Hypertension (Dallas, Tex. 1979), 2010-06, Vol.55 (6), p.1412-1417 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Analysis of Variance Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Biomarkers - metabolism Blood and lymphatic vessels Blood Pressure Determination Cardiology. Vascular system Cardiomyopathy, Hypertrophic - diagnostic imaging Cardiomyopathy, Hypertrophic - metabolism Cardiomyopathy, Hypertrophic - physiopathology Disease Models, Animal Echocardiography Female Ferritins - metabolism Gene Expression Regulation Glutathione Peroxidase - genetics Glutathione Peroxidase - metabolism Heart Heart Function Tests HSP27 Heat-Shock Proteins - genetics HSP27 Heat-Shock Proteins - metabolism Immunohistochemistry Male Medical sciences Mice Mice, Transgenic Myocarditis. Cardiomyopathies Myocytes, Cardiac - pathology Myocytes, Cardiac - ultrastructure Oxidative Stress - physiology Random Allocation Reference Values Up-Regulation |
| title | Involvement of Reductive Stress in the Cardiomyopathy in Transgenic Mice With Cardiac-Specific Overexpression of Heat Shock Protein 27 |
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