Proteomic analysis of left ventricular diastolic dysfunction hearts in renovascular hypertensive rats
Abstract Abnormalities of diastolic function are common to virtually all forms of cardiac failure. However, the molecular events leading to diastolic dysfunction have not been fully elucidated. We performed a differential proteomic profiling study on diastolic dysfunction hearts induced by renovascu...
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| Veröffentlicht in: | International journal of cardiology 2008-07, Vol.127 (2), p.198-207 |
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| creator | Junhong, Wang Jing, Yang Jizheng, Ma Shushu, Zhu Xiangjian, Chen Hengfang, Wu Di, Yang Jinan, Zhang |
| description | Abstract Abnormalities of diastolic function are common to virtually all forms of cardiac failure. However, the molecular events leading to diastolic dysfunction have not been fully elucidated. We performed a differential proteomic profiling study on diastolic dysfunction hearts induced by renovascular hypertension. Left ventricular diastolic dysfunction induced by renovascular hypertension (2K1C, two-kidneys, one clip) was performed in twelve Sprague–Dawley rats. 2D echocardiographic and cardiac protein patterns (2D-electrophoresis and mass spectroscopy) were compared with the sham operated rats. We described sixteen altered protein spots in 2K1C rats with left ventricular diastolic dysfunction. Calsarcin-1 (CS-1) was significantly down-regulated in 2K1C rats and it showed a negative correlation with calcineurin enzymatic activity ( r2 = 0.72 p = 0.03). We also showed changes in cellular energy metabolism in 2K1C rats, and these changes go in parallel with alterations of the thin filament proteome responsible for actin-myosin cross-bridge. In conclusion, this study provides a new insight into the left ventricular proteome profile associated with systemic hypertension induced diastolic dysfunction in a renovascular hypertension rat model. The decreased CS-1 protein with a concomitant increased enzymatic activity of calcineurin, suggests an important role of CS-1 in the calcineurin-mediated left ventricular hypertrophy. |
| doi_str_mv | 10.1016/j.ijcard.2007.07.003 |
| format | Article |
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However, the molecular events leading to diastolic dysfunction have not been fully elucidated. We performed a differential proteomic profiling study on diastolic dysfunction hearts induced by renovascular hypertension. Left ventricular diastolic dysfunction induced by renovascular hypertension (2K1C, two-kidneys, one clip) was performed in twelve Sprague–Dawley rats. 2D echocardiographic and cardiac protein patterns (2D-electrophoresis and mass spectroscopy) were compared with the sham operated rats. We described sixteen altered protein spots in 2K1C rats with left ventricular diastolic dysfunction. Calsarcin-1 (CS-1) was significantly down-regulated in 2K1C rats and it showed a negative correlation with calcineurin enzymatic activity ( r2 = 0.72 p = 0.03). We also showed changes in cellular energy metabolism in 2K1C rats, and these changes go in parallel with alterations of the thin filament proteome responsible for actin-myosin cross-bridge. In conclusion, this study provides a new insight into the left ventricular proteome profile associated with systemic hypertension induced diastolic dysfunction in a renovascular hypertension rat model. The decreased CS-1 protein with a concomitant increased enzymatic activity of calcineurin, suggests an important role of CS-1 in the calcineurin-mediated left ventricular hypertrophy.</description><identifier>ISSN: 0167-5273</identifier><identifier>EISSN: 1874-1754</identifier><identifier>DOI: 10.1016/j.ijcard.2007.07.003</identifier><identifier>PMID: 17659790</identifier><identifier>CODEN: IJCDD5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Animals ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blotting, Western ; Calcineurin - metabolism ; Cardiology. Vascular system ; Cardiovascular ; Echocardiography ; Heart ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Heart Failure, Diastolic - etiology ; Heart Failure, Diastolic - metabolism ; Heart Failure, Diastolic - physiopathology ; Hypertension, Renovascular - complications ; Male ; Mass Spectrometry ; Medical sciences ; Pathophysiology ; Proteome - analysis ; Proteomics ; Proteomics - methods ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Statistics, Nonparametric ; Ventricular dysfunction ; Ventricular Dysfunction, Left - etiology ; Ventricular Dysfunction, Left - metabolism ; Ventricular Dysfunction, Left - physiopathology</subject><ispartof>International journal of cardiology, 2008-07, Vol.127 (2), p.198-207</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2007 Elsevier Ireland Ltd</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c445t-b22b900e9579477cc8496c2a2936423209186301e75d474893748ee8962a5e543</citedby><cites>FETCH-LOGICAL-c445t-b22b900e9579477cc8496c2a2936423209186301e75d474893748ee8962a5e543</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S016752730701039X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20443749$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17659790$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Junhong, Wang</creatorcontrib><creatorcontrib>Jing, Yang</creatorcontrib><creatorcontrib>Jizheng, Ma</creatorcontrib><creatorcontrib>Shushu, Zhu</creatorcontrib><creatorcontrib>Xiangjian, Chen</creatorcontrib><creatorcontrib>Hengfang, Wu</creatorcontrib><creatorcontrib>Di, Yang</creatorcontrib><creatorcontrib>Jinan, Zhang</creatorcontrib><title>Proteomic analysis of left ventricular diastolic dysfunction hearts in renovascular hypertensive rats</title><title>International journal of cardiology</title><addtitle>Int J Cardiol</addtitle><description>Abstract Abnormalities of diastolic function are common to virtually all forms of cardiac failure. However, the molecular events leading to diastolic dysfunction have not been fully elucidated. We performed a differential proteomic profiling study on diastolic dysfunction hearts induced by renovascular hypertension. Left ventricular diastolic dysfunction induced by renovascular hypertension (2K1C, two-kidneys, one clip) was performed in twelve Sprague–Dawley rats. 2D echocardiographic and cardiac protein patterns (2D-electrophoresis and mass spectroscopy) were compared with the sham operated rats. We described sixteen altered protein spots in 2K1C rats with left ventricular diastolic dysfunction. Calsarcin-1 (CS-1) was significantly down-regulated in 2K1C rats and it showed a negative correlation with calcineurin enzymatic activity ( r2 = 0.72 p = 0.03). We also showed changes in cellular energy metabolism in 2K1C rats, and these changes go in parallel with alterations of the thin filament proteome responsible for actin-myosin cross-bridge. In conclusion, this study provides a new insight into the left ventricular proteome profile associated with systemic hypertension induced diastolic dysfunction in a renovascular hypertension rat model. The decreased CS-1 protein with a concomitant increased enzymatic activity of calcineurin, suggests an important role of CS-1 in the calcineurin-mediated left ventricular hypertrophy.</description><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blotting, Western</subject><subject>Calcineurin - metabolism</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular</subject><subject>Echocardiography</subject><subject>Heart</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Heart Failure, Diastolic - etiology</subject><subject>Heart Failure, Diastolic - metabolism</subject><subject>Heart Failure, Diastolic - physiopathology</subject><subject>Hypertension, Renovascular - complications</subject><subject>Male</subject><subject>Mass Spectrometry</subject><subject>Medical sciences</subject><subject>Pathophysiology</subject><subject>Proteome - analysis</subject><subject>Proteomics</subject><subject>Proteomics - methods</subject><subject>Random Allocation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Statistics, Nonparametric</subject><subject>Ventricular dysfunction</subject><subject>Ventricular Dysfunction, Left - etiology</subject><subject>Ventricular Dysfunction, Left - metabolism</subject><subject>Ventricular Dysfunction, Left - physiopathology</subject><issn>0167-5273</issn><issn>1874-1754</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFklGL1DAQx4Mo3t7pNxDpi751TdKkaV4EOdQTDhRU8C1k0ymX2k3WTLrQb29KFwVfhCF5-c0_wy9DyAtG94yy9s2496Ozqd9zStV-Ldo8IjvWKVEzJcVjsiuYqiVXzRW5RhwppULr7im5YqqVWmm6I_AlxQzx6F1lg50W9FjFoZpgyNUZQk7ezZNNVe8t5jgVrF9wmIPLPobqAWzKWPlQJQjxbHGDH5YTpAwB_RmqZDM-I08GOyE8v9w35PuH999u7-r7zx8_3b67r50QMtcHzg-aUtBSaaGUc53QreOW66YVvOFUs65tKAMle6FEp5tyAHS65VaCFM0Neb3lnlL8NQNmc_ToYJpsgDijaTVnXEtZQLGBLkXEBIM5JX-0aTGMmlWvGc2m16x6zVq0KW0vL_nz4Qj936aLzwK8ugDFhZ2GZIPz-IfjVIgysy7c242DYuPsIRl0HoKD3idw2fTR_2-SfwPc5IMvb_6EBXCMcyrfiYYZ5Iaar-sqrJtAFWW00T-a33ZWr9s</recordid><startdate>20080704</startdate><enddate>20080704</enddate><creator>Junhong, Wang</creator><creator>Jing, Yang</creator><creator>Jizheng, Ma</creator><creator>Shushu, Zhu</creator><creator>Xiangjian, Chen</creator><creator>Hengfang, Wu</creator><creator>Di, Yang</creator><creator>Jinan, Zhang</creator><general>Elsevier Ireland Ltd</general><general>Elsevier Science</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>20080704</creationdate><title>Proteomic analysis of left ventricular diastolic dysfunction hearts in renovascular hypertensive rats</title><author>Junhong, Wang ; Jing, Yang ; Jizheng, Ma ; Shushu, Zhu ; Xiangjian, Chen ; Hengfang, Wu ; Di, Yang ; Jinan, Zhang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c445t-b22b900e9579477cc8496c2a2936423209186301e75d474893748ee8962a5e543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blotting, Western</topic><topic>Calcineurin - metabolism</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular</topic><topic>Echocardiography</topic><topic>Heart</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Heart Failure, Diastolic - etiology</topic><topic>Heart Failure, Diastolic - metabolism</topic><topic>Heart Failure, Diastolic - physiopathology</topic><topic>Hypertension, Renovascular - complications</topic><topic>Male</topic><topic>Mass Spectrometry</topic><topic>Medical sciences</topic><topic>Pathophysiology</topic><topic>Proteome - analysis</topic><topic>Proteomics</topic><topic>Proteomics - methods</topic><topic>Random Allocation</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Statistics, Nonparametric</topic><topic>Ventricular dysfunction</topic><topic>Ventricular Dysfunction, Left - etiology</topic><topic>Ventricular Dysfunction, Left - metabolism</topic><topic>Ventricular Dysfunction, Left - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Junhong, Wang</creatorcontrib><creatorcontrib>Jing, Yang</creatorcontrib><creatorcontrib>Jizheng, Ma</creatorcontrib><creatorcontrib>Shushu, Zhu</creatorcontrib><creatorcontrib>Xiangjian, Chen</creatorcontrib><creatorcontrib>Hengfang, Wu</creatorcontrib><creatorcontrib>Di, Yang</creatorcontrib><creatorcontrib>Jinan, Zhang</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>International journal of cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Junhong, Wang</au><au>Jing, Yang</au><au>Jizheng, Ma</au><au>Shushu, Zhu</au><au>Xiangjian, Chen</au><au>Hengfang, Wu</au><au>Di, Yang</au><au>Jinan, Zhang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Proteomic analysis of left ventricular diastolic dysfunction hearts in renovascular hypertensive rats</atitle><jtitle>International journal of cardiology</jtitle><addtitle>Int J Cardiol</addtitle><date>2008-07-04</date><risdate>2008</risdate><volume>127</volume><issue>2</issue><spage>198</spage><epage>207</epage><pages>198-207</pages><issn>0167-5273</issn><eissn>1874-1754</eissn><coden>IJCDD5</coden><abstract>Abstract Abnormalities of diastolic function are common to virtually all forms of cardiac failure. However, the molecular events leading to diastolic dysfunction have not been fully elucidated. We performed a differential proteomic profiling study on diastolic dysfunction hearts induced by renovascular hypertension. Left ventricular diastolic dysfunction induced by renovascular hypertension (2K1C, two-kidneys, one clip) was performed in twelve Sprague–Dawley rats. 2D echocardiographic and cardiac protein patterns (2D-electrophoresis and mass spectroscopy) were compared with the sham operated rats. We described sixteen altered protein spots in 2K1C rats with left ventricular diastolic dysfunction. Calsarcin-1 (CS-1) was significantly down-regulated in 2K1C rats and it showed a negative correlation with calcineurin enzymatic activity ( r2 = 0.72 p = 0.03). We also showed changes in cellular energy metabolism in 2K1C rats, and these changes go in parallel with alterations of the thin filament proteome responsible for actin-myosin cross-bridge. In conclusion, this study provides a new insight into the left ventricular proteome profile associated with systemic hypertension induced diastolic dysfunction in a renovascular hypertension rat model. The decreased CS-1 protein with a concomitant increased enzymatic activity of calcineurin, suggests an important role of CS-1 in the calcineurin-mediated left ventricular hypertrophy.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>17659790</pmid><doi>10.1016/j.ijcard.2007.07.003</doi><tpages>10</tpages></addata></record> |
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| subjects | Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blotting, Western Calcineurin - metabolism Cardiology. Vascular system Cardiovascular Echocardiography Heart Heart failure, cardiogenic pulmonary edema, cardiac enlargement Heart Failure, Diastolic - etiology Heart Failure, Diastolic - metabolism Heart Failure, Diastolic - physiopathology Hypertension, Renovascular - complications Male Mass Spectrometry Medical sciences Pathophysiology Proteome - analysis Proteomics Proteomics - methods Random Allocation Rats Rats, Sprague-Dawley Reverse Transcriptase Polymerase Chain Reaction Statistics, Nonparametric Ventricular dysfunction Ventricular Dysfunction, Left - etiology Ventricular Dysfunction, Left - metabolism Ventricular Dysfunction, Left - physiopathology |
| title | Proteomic analysis of left ventricular diastolic dysfunction hearts in renovascular hypertensive rats |
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