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Chronic Phospholamban–Sarcoplasmic Reticulum Calcium ATPase Interaction Is the Critical Calcium Cycling Defect in Dilated Cardiomyopathy
Dilated cardiomyopathy and end-stage heart failure result in multiple defects in cardiac excitation–contraction coupling. Via complementation of a genetically based mouse model of dilated cardiomyopathy, we now provide evidence that progressive chamber dilation and heart failure are dependent on a C...
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| Published in: | Cell 1999-10, Vol.99 (3), p.313-322 |
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| Main Authors: | , , , , , , , , , , , |
| Format: | Article |
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| container_end_page | 322 |
| container_issue | 3 |
| container_start_page | 313 |
| container_title | Cell |
| container_volume | 99 |
| creator | Minamisawa, Susumu Hoshijima, Masahiko Chu, Guoxiang Ward, Christopher A Frank, Konrad Gu, Yusu Martone, Maryann E Wang, Yibin Ross, John Kranias, Evangelia G Giles, Wayne R Chien, Kenneth R |
| description | Dilated cardiomyopathy and end-stage heart failure result in multiple defects in cardiac excitation–contraction coupling. Via complementation of a genetically based mouse model of dilated cardiomyopathy, we now provide evidence that progressive chamber dilation and heart failure are dependent on a Ca
2+ cycling defect in the cardiac sarcoplasmic reticulum. The ablation of a muscle-specific sarcoplasmic reticulum Ca
2+ ATPase (SERCA2a) inhibitor, phospholamban, rescued the spectrum of phenotypes that resemble human heart failure. Inhibition of phospholamban–SERCA2a interaction via in vivo expression of a phospholamban point mutant dominantly activated the contractility of ventricular muscle cells. Thus, interfering with phospholamban–SERCA2a interaction may provide a novel therapeutic approach for preventing the progression of dilated cardiomyopathy. |
| doi_str_mv | 10.1016/S0092-8674(00)81662-1 |
| format | article |
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2+ cycling defect in the cardiac sarcoplasmic reticulum. The ablation of a muscle-specific sarcoplasmic reticulum Ca
2+ ATPase (SERCA2a) inhibitor, phospholamban, rescued the spectrum of phenotypes that resemble human heart failure. Inhibition of phospholamban–SERCA2a interaction via in vivo expression of a phospholamban point mutant dominantly activated the contractility of ventricular muscle cells. Thus, interfering with phospholamban–SERCA2a interaction may provide a novel therapeutic approach for preventing the progression of dilated cardiomyopathy.</description><identifier>ISSN: 0092-8674</identifier><identifier>EISSN: 1097-4172</identifier><identifier>DOI: 10.1016/S0092-8674(00)81662-1</identifier><identifier>PMID: 10555147</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Calcium - metabolism ; Calcium-Binding Proteins - deficiency ; Calcium-Binding Proteins - genetics ; Calcium-Binding Proteins - metabolism ; Calcium-Transporting ATPases - antagonists & inhibitors ; Calcium-Transporting ATPases - metabolism ; Cardiomyopathy, Dilated - genetics ; Cardiomyopathy, Dilated - pathology ; Cardiomyopathy, Dilated - physiopathology ; Disease Models, Animal ; Disease Progression ; Heart - physiology ; Heart - physiopathology ; Hemodynamics - genetics ; Hemodynamics - physiology ; Homeostasis ; Humans ; Mice ; Mice, Knockout ; Myocardial Contraction ; Myocardium - pathology ; phospholamban ; Sarcoplasmic Reticulum - enzymology ; Ventricular Function, Left</subject><ispartof>Cell, 1999-10, Vol.99 (3), p.313-322</ispartof><rights>1999 Cell Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c557t-cfd40058df1fcb33d0fcf1d744ba756249ba388f1f0e4febecd7ba9c1e060ca03</citedby><cites>FETCH-LOGICAL-c557t-cfd40058df1fcb33d0fcf1d744ba756249ba388f1f0e4febecd7ba9c1e060ca03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10555147$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Minamisawa, Susumu</creatorcontrib><creatorcontrib>Hoshijima, Masahiko</creatorcontrib><creatorcontrib>Chu, Guoxiang</creatorcontrib><creatorcontrib>Ward, Christopher A</creatorcontrib><creatorcontrib>Frank, Konrad</creatorcontrib><creatorcontrib>Gu, Yusu</creatorcontrib><creatorcontrib>Martone, Maryann E</creatorcontrib><creatorcontrib>Wang, Yibin</creatorcontrib><creatorcontrib>Ross, John</creatorcontrib><creatorcontrib>Kranias, Evangelia G</creatorcontrib><creatorcontrib>Giles, Wayne R</creatorcontrib><creatorcontrib>Chien, Kenneth R</creatorcontrib><title>Chronic Phospholamban–Sarcoplasmic Reticulum Calcium ATPase Interaction Is the Critical Calcium Cycling Defect in Dilated Cardiomyopathy</title><title>Cell</title><addtitle>Cell</addtitle><description>Dilated cardiomyopathy and end-stage heart failure result in multiple defects in cardiac excitation–contraction coupling. Via complementation of a genetically based mouse model of dilated cardiomyopathy, we now provide evidence that progressive chamber dilation and heart failure are dependent on a Ca
2+ cycling defect in the cardiac sarcoplasmic reticulum. The ablation of a muscle-specific sarcoplasmic reticulum Ca
2+ ATPase (SERCA2a) inhibitor, phospholamban, rescued the spectrum of phenotypes that resemble human heart failure. Inhibition of phospholamban–SERCA2a interaction via in vivo expression of a phospholamban point mutant dominantly activated the contractility of ventricular muscle cells. Thus, interfering with phospholamban–SERCA2a interaction may provide a novel therapeutic approach for preventing the progression of dilated cardiomyopathy.</description><subject>Animals</subject><subject>Calcium - metabolism</subject><subject>Calcium-Binding Proteins - deficiency</subject><subject>Calcium-Binding Proteins - genetics</subject><subject>Calcium-Binding Proteins - metabolism</subject><subject>Calcium-Transporting ATPases - antagonists & inhibitors</subject><subject>Calcium-Transporting ATPases - metabolism</subject><subject>Cardiomyopathy, Dilated - genetics</subject><subject>Cardiomyopathy, Dilated - pathology</subject><subject>Cardiomyopathy, Dilated - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Heart - physiology</subject><subject>Heart - physiopathology</subject><subject>Hemodynamics - genetics</subject><subject>Hemodynamics - physiology</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Myocardial Contraction</subject><subject>Myocardium - pathology</subject><subject>phospholamban</subject><subject>Sarcoplasmic Reticulum - enzymology</subject><subject>Ventricular Function, Left</subject><issn>0092-8674</issn><issn>1097-4172</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><recordid>eNqFkc1u1TAQRi1ERS-FRwBlhWARGOfHTlaoSqFcqRIVLWvLscfEyImDnSDdHWu2vCFPUt_eququq28x55uR5hDyisJ7CpR9uAJoi7xhvHoL8K6hjBU5fUI2FFqeV5QXT8nmHjkmz2P8CQBNXdfPyDGFlLTiG_K3G4KfrMouBx_nwTs59nL6_-fflQzKz07GMQ2_4WLV6tYx66RTNuXp9aWMmG2nBYNUi_VTto3ZMmDWBZtg6e7RbqecnX5kZ2hQLZmdsjPr5II6EUFbP-78LJdh94IcGekivrzLE_L986fr7kt-8fV8251e5Kqu-ZIroyuAutGGGtWXpQajDNW8qnrJa1ZUbS_LpklTwMpgj0rzXraKIjBQEsoT8uawdw7-14pxEaONCp2TE_o1CtYWrISCPgpSXjfA2B6sD6AKPsaARszBjjLsBAWxtyVubYm9CgEgbm2Jfe_13YG1H1E_aB30JODjAcD0j98Wg4jK4qRQ25B-KbS3j5y4AbIBqHI</recordid><startdate>19991029</startdate><enddate>19991029</enddate><creator>Minamisawa, Susumu</creator><creator>Hoshijima, Masahiko</creator><creator>Chu, Guoxiang</creator><creator>Ward, Christopher A</creator><creator>Frank, Konrad</creator><creator>Gu, Yusu</creator><creator>Martone, Maryann E</creator><creator>Wang, Yibin</creator><creator>Ross, John</creator><creator>Kranias, Evangelia G</creator><creator>Giles, Wayne R</creator><creator>Chien, Kenneth R</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</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>7QP</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>19991029</creationdate><title>Chronic Phospholamban–Sarcoplasmic Reticulum Calcium ATPase Interaction Is the Critical Calcium Cycling Defect in Dilated Cardiomyopathy</title><author>Minamisawa, Susumu ; Hoshijima, Masahiko ; Chu, Guoxiang ; Ward, Christopher A ; Frank, Konrad ; Gu, Yusu ; Martone, Maryann E ; Wang, Yibin ; Ross, John ; Kranias, Evangelia G ; Giles, Wayne R ; Chien, Kenneth R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c557t-cfd40058df1fcb33d0fcf1d744ba756249ba388f1f0e4febecd7ba9c1e060ca03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Calcium - metabolism</topic><topic>Calcium-Binding Proteins - deficiency</topic><topic>Calcium-Binding Proteins - genetics</topic><topic>Calcium-Binding Proteins - metabolism</topic><topic>Calcium-Transporting ATPases - antagonists & inhibitors</topic><topic>Calcium-Transporting ATPases - metabolism</topic><topic>Cardiomyopathy, Dilated - genetics</topic><topic>Cardiomyopathy, Dilated - pathology</topic><topic>Cardiomyopathy, Dilated - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>Heart - physiology</topic><topic>Heart - physiopathology</topic><topic>Hemodynamics - genetics</topic><topic>Hemodynamics - physiology</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Myocardial Contraction</topic><topic>Myocardium - pathology</topic><topic>phospholamban</topic><topic>Sarcoplasmic Reticulum - enzymology</topic><topic>Ventricular Function, Left</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Minamisawa, Susumu</creatorcontrib><creatorcontrib>Hoshijima, Masahiko</creatorcontrib><creatorcontrib>Chu, Guoxiang</creatorcontrib><creatorcontrib>Ward, Christopher A</creatorcontrib><creatorcontrib>Frank, Konrad</creatorcontrib><creatorcontrib>Gu, Yusu</creatorcontrib><creatorcontrib>Martone, Maryann E</creatorcontrib><creatorcontrib>Wang, Yibin</creatorcontrib><creatorcontrib>Ross, John</creatorcontrib><creatorcontrib>Kranias, Evangelia G</creatorcontrib><creatorcontrib>Giles, Wayne R</creatorcontrib><creatorcontrib>Chien, Kenneth R</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Minamisawa, Susumu</au><au>Hoshijima, Masahiko</au><au>Chu, Guoxiang</au><au>Ward, Christopher A</au><au>Frank, Konrad</au><au>Gu, Yusu</au><au>Martone, Maryann E</au><au>Wang, Yibin</au><au>Ross, John</au><au>Kranias, Evangelia G</au><au>Giles, Wayne R</au><au>Chien, Kenneth R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic Phospholamban–Sarcoplasmic Reticulum Calcium ATPase Interaction Is the Critical Calcium Cycling Defect in Dilated Cardiomyopathy</atitle><jtitle>Cell</jtitle><addtitle>Cell</addtitle><date>1999-10-29</date><risdate>1999</risdate><volume>99</volume><issue>3</issue><spage>313</spage><epage>322</epage><pages>313-322</pages><issn>0092-8674</issn><eissn>1097-4172</eissn><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-1</notes><notes>content type line 23</notes><notes>ObjectType-Article-1</notes><notes>ObjectType-Feature-2</notes><abstract>Dilated cardiomyopathy and end-stage heart failure result in multiple defects in cardiac excitation–contraction coupling. Via complementation of a genetically based mouse model of dilated cardiomyopathy, we now provide evidence that progressive chamber dilation and heart failure are dependent on a Ca
2+ cycling defect in the cardiac sarcoplasmic reticulum. The ablation of a muscle-specific sarcoplasmic reticulum Ca
2+ ATPase (SERCA2a) inhibitor, phospholamban, rescued the spectrum of phenotypes that resemble human heart failure. Inhibition of phospholamban–SERCA2a interaction via in vivo expression of a phospholamban point mutant dominantly activated the contractility of ventricular muscle cells. Thus, interfering with phospholamban–SERCA2a interaction may provide a novel therapeutic approach for preventing the progression of dilated cardiomyopathy.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>10555147</pmid><doi>10.1016/S0092-8674(00)81662-1</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cell, 1999-10, Vol.99 (3), p.313-322 |
| issn | 0092-8674 1097-4172 |
| language | eng |
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| source | BACON - Elsevier - GLOBAL_SCIENCEDIRECT-OPENACCESS |
| subjects | Animals Calcium - metabolism Calcium-Binding Proteins - deficiency Calcium-Binding Proteins - genetics Calcium-Binding Proteins - metabolism Calcium-Transporting ATPases - antagonists & inhibitors Calcium-Transporting ATPases - metabolism Cardiomyopathy, Dilated - genetics Cardiomyopathy, Dilated - pathology Cardiomyopathy, Dilated - physiopathology Disease Models, Animal Disease Progression Heart - physiology Heart - physiopathology Hemodynamics - genetics Hemodynamics - physiology Homeostasis Humans Mice Mice, Knockout Myocardial Contraction Myocardium - pathology phospholamban Sarcoplasmic Reticulum - enzymology Ventricular Function, Left |
| title | Chronic Phospholamban–Sarcoplasmic Reticulum Calcium ATPase Interaction Is the Critical Calcium Cycling Defect in Dilated Cardiomyopathy |
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