Sexually dimorphic myofilament function and cardiac troponin I phosphospecies distribution in hypertrophic cardiomyopathy mice
► 10–12Month HCM females develop proportionately larger hearts than HCM males. ► HCM females display alterations in Ca2+-sensitivity over female WT; HCM males do not. ► The pattern of cTnI post-translational modification depends on sex and HCM genotype. The pathological progression of hypertrophic c...
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| Veröffentlicht in: | Archives of biochemistry and biophysics 2013-07, Vol.535 (1), p.39-48 |
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| creator | McKee, Laurel A.K. Chen, Hao Regan, Jessica A. Behunin, Samantha M. Walker, Jeffery W. Walker, John S. Konhilas, John P. |
| description | ► 10–12Month HCM females develop proportionately larger hearts than HCM males. ► HCM females display alterations in Ca2+-sensitivity over female WT; HCM males do not. ► The pattern of cTnI post-translational modification depends on sex and HCM genotype.
The pathological progression of hypertrophic cardiomyopathy (HCM) is sexually dimorphic such that male HCM mice develop phenotypic indicators of cardiac disease well before female HCM mice. Here, we hypothesized that alterations in myofilament function underlies, in part, this sex dimorphism in HCM disease development. Firstly, 10–12month female HCM (harboring a mutant [R403Q] myosin heavy chain) mice presented with proportionately larger hearts than male HCM mice. Next, we determined Ca2+-sensitive tension development in demembranated cardiac trabeculae excised from 10–12month female and male HCM mice. Whereas HCM did not impact Ca2+-sensitive tension development in male trabeculae, female HCM trabeculae were more sensitive to Ca2+ than wild-type (WT) counterparts and both WT and HCM males. We hypothesized that the underlying cause of this sex difference in Ca2+-sensitive tension development was due to changes in Ca2+ handling and sarcomeric proteins, including expression of SR Ca2+ ATPase (2a) (SERCA2a), β-myosin heavy chain (β-MyHC) and post-translational modifications of myofilament proteins. Female HCM hearts showed an elevation of SERCA2a and β-MyHC protein whereas male HCM hearts showed a similar elevation of β-MyHC protein but a reduced level of cardiac troponin T (cTnT) phosphorylation. We also measured the distribution of cardiac troponin I (cTnI) phosphospecies using phosphate-affinity SDS–PAGE. The distribution of cTnI phosphospecies depended on sex and HCM. In conclusion, female and male HCM mice display sex dimorphic myofilament function that is accompanied by a sex- and HCM-dependent distribution of sarcomeric proteins and cTnI phosphospecies. |
| doi_str_mv | 10.1016/j.abb.2012.12.023 |
| format | Article |
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The pathological progression of hypertrophic cardiomyopathy (HCM) is sexually dimorphic such that male HCM mice develop phenotypic indicators of cardiac disease well before female HCM mice. Here, we hypothesized that alterations in myofilament function underlies, in part, this sex dimorphism in HCM disease development. Firstly, 10–12month female HCM (harboring a mutant [R403Q] myosin heavy chain) mice presented with proportionately larger hearts than male HCM mice. Next, we determined Ca2+-sensitive tension development in demembranated cardiac trabeculae excised from 10–12month female and male HCM mice. Whereas HCM did not impact Ca2+-sensitive tension development in male trabeculae, female HCM trabeculae were more sensitive to Ca2+ than wild-type (WT) counterparts and both WT and HCM males. We hypothesized that the underlying cause of this sex difference in Ca2+-sensitive tension development was due to changes in Ca2+ handling and sarcomeric proteins, including expression of SR Ca2+ ATPase (2a) (SERCA2a), β-myosin heavy chain (β-MyHC) and post-translational modifications of myofilament proteins. Female HCM hearts showed an elevation of SERCA2a and β-MyHC protein whereas male HCM hearts showed a similar elevation of β-MyHC protein but a reduced level of cardiac troponin T (cTnT) phosphorylation. We also measured the distribution of cardiac troponin I (cTnI) phosphospecies using phosphate-affinity SDS–PAGE. The distribution of cTnI phosphospecies depended on sex and HCM. In conclusion, female and male HCM mice display sex dimorphic myofilament function that is accompanied by a sex- and HCM-dependent distribution of sarcomeric proteins and cTnI phosphospecies.</description><identifier>ISSN: 0003-9861</identifier><identifier>EISSN: 1096-0384</identifier><identifier>DOI: 10.1016/j.abb.2012.12.023</identifier><identifier>PMID: 23352598</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>adenosinetriphosphatase ; Animals ; Ca2-transporting ATPase ; calcium ; Calcium - metabolism ; cardiomyopathy ; Cardiomyopathy, Hypertrophic - enzymology ; Cardiomyopathy, Hypertrophic - metabolism ; Cardiomyopathy, Hypertrophic - pathology ; cTnI ; dimorphism ; Electrophoresis, Polyacrylamide Gel ; Female ; females ; Heart Ventricles - metabolism ; Heart Ventricles - pathology ; Hypertrophic cardiomyopathy ; Male ; males ; Mice ; Muscle Tonus ; mutants ; Mutation ; Myofibrils - genetics ; Myofibrils - metabolism ; Myofibrils - physiology ; myosin heavy chains ; Myosin Heavy Chains - metabolism ; Myosin Light Chains - metabolism ; Phosphate-affinity SDS–PAGE ; Phosphorylation ; polyacrylamide gel electrophoresis ; post-translational modification ; Protein Processing, Post-Translational ; Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics ; Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism ; Sex Factors ; Site-specific phosphorylation ; SR Ca2+ ATPase (2a) (SERCA2a) ; troponin I ; Troponin I - metabolism ; troponin T ; Troponin T - metabolism ; Ventricular Myosins - genetics ; Ventricular Myosins - metabolism</subject><ispartof>Archives of biochemistry and biophysics, 2013-07, Vol.535 (1), p.39-48</ispartof><rights>2013 Elsevier Inc.</rights><rights>Copyright © 2013 Elsevier Inc. All rights reserved.</rights><rights>2013 Published by Elsevier Inc. 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c574t-ba907224b78de9aa1983f7e90502dcd7c9fdd38da18929a52737ac9be3a1bc673</citedby><cites>FETCH-LOGICAL-c574t-ba907224b78de9aa1983f7e90502dcd7c9fdd38da18929a52737ac9be3a1bc673</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.abb.2012.12.023$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,777,781,882,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23352598$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McKee, Laurel A.K.</creatorcontrib><creatorcontrib>Chen, Hao</creatorcontrib><creatorcontrib>Regan, Jessica A.</creatorcontrib><creatorcontrib>Behunin, Samantha M.</creatorcontrib><creatorcontrib>Walker, Jeffery W.</creatorcontrib><creatorcontrib>Walker, John S.</creatorcontrib><creatorcontrib>Konhilas, John P.</creatorcontrib><title>Sexually dimorphic myofilament function and cardiac troponin I phosphospecies distribution in hypertrophic cardiomyopathy mice</title><title>Archives of biochemistry and biophysics</title><addtitle>Arch Biochem Biophys</addtitle><description>► 10–12Month HCM females develop proportionately larger hearts than HCM males. ► HCM females display alterations in Ca2+-sensitivity over female WT; HCM males do not. ► The pattern of cTnI post-translational modification depends on sex and HCM genotype.
The pathological progression of hypertrophic cardiomyopathy (HCM) is sexually dimorphic such that male HCM mice develop phenotypic indicators of cardiac disease well before female HCM mice. Here, we hypothesized that alterations in myofilament function underlies, in part, this sex dimorphism in HCM disease development. Firstly, 10–12month female HCM (harboring a mutant [R403Q] myosin heavy chain) mice presented with proportionately larger hearts than male HCM mice. Next, we determined Ca2+-sensitive tension development in demembranated cardiac trabeculae excised from 10–12month female and male HCM mice. Whereas HCM did not impact Ca2+-sensitive tension development in male trabeculae, female HCM trabeculae were more sensitive to Ca2+ than wild-type (WT) counterparts and both WT and HCM males. We hypothesized that the underlying cause of this sex difference in Ca2+-sensitive tension development was due to changes in Ca2+ handling and sarcomeric proteins, including expression of SR Ca2+ ATPase (2a) (SERCA2a), β-myosin heavy chain (β-MyHC) and post-translational modifications of myofilament proteins. Female HCM hearts showed an elevation of SERCA2a and β-MyHC protein whereas male HCM hearts showed a similar elevation of β-MyHC protein but a reduced level of cardiac troponin T (cTnT) phosphorylation. We also measured the distribution of cardiac troponin I (cTnI) phosphospecies using phosphate-affinity SDS–PAGE. The distribution of cTnI phosphospecies depended on sex and HCM. In conclusion, female and male HCM mice display sex dimorphic myofilament function that is accompanied by a sex- and HCM-dependent distribution of sarcomeric proteins and cTnI phosphospecies.</description><subject>adenosinetriphosphatase</subject><subject>Animals</subject><subject>Ca2-transporting ATPase</subject><subject>calcium</subject><subject>Calcium - metabolism</subject><subject>cardiomyopathy</subject><subject>Cardiomyopathy, Hypertrophic - enzymology</subject><subject>Cardiomyopathy, Hypertrophic - metabolism</subject><subject>Cardiomyopathy, Hypertrophic - pathology</subject><subject>cTnI</subject><subject>dimorphism</subject><subject>Electrophoresis, Polyacrylamide Gel</subject><subject>Female</subject><subject>females</subject><subject>Heart Ventricles - metabolism</subject><subject>Heart Ventricles - pathology</subject><subject>Hypertrophic cardiomyopathy</subject><subject>Male</subject><subject>males</subject><subject>Mice</subject><subject>Muscle Tonus</subject><subject>mutants</subject><subject>Mutation</subject><subject>Myofibrils - genetics</subject><subject>Myofibrils - metabolism</subject><subject>Myofibrils - physiology</subject><subject>myosin heavy chains</subject><subject>Myosin Heavy Chains - metabolism</subject><subject>Myosin Light Chains - metabolism</subject><subject>Phosphate-affinity SDS–PAGE</subject><subject>Phosphorylation</subject><subject>polyacrylamide gel electrophoresis</subject><subject>post-translational modification</subject><subject>Protein Processing, Post-Translational</subject><subject>Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics</subject><subject>Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism</subject><subject>Sex Factors</subject><subject>Site-specific phosphorylation</subject><subject>SR Ca2+ ATPase (2a) (SERCA2a)</subject><subject>troponin I</subject><subject>Troponin I - metabolism</subject><subject>troponin T</subject><subject>Troponin T - metabolism</subject><subject>Ventricular Myosins - genetics</subject><subject>Ventricular Myosins - metabolism</subject><issn>0003-9861</issn><issn>1096-0384</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU2L1TAUhoMoznX0B7jRLt30ms-mQRBk8GNgwMU463CapNNc2qYm7WA3_nbTe8dBNwonZJHnPJyTF6GXBO8JJtXbwx6aZk8xoftcmLJHaEewqkrMav4Y7TDGrFR1Rc7Qs5QOGBPCK_oUnVHGBBWq3qGf1-7HAn2_FtYPIU6dN8Wwhtb3MLhxLtplNLMPYwGjLQxE68EUcwxTGP1YXBZTF9LxOONdypI0R98sx5YMdOvk4oZv3mN7yPYJ5m4tBm_cc_SkhT65F_f3Obr59PHbxZfy6uvny4sPV6URks9lAwpLSnkja-sUAFE1a6VTWGBqjZVGtday2gKpFVUgqGQSjGocA9KYSrJz9P7knZZmcNbk1SL0eop-gLjqAF7__TL6Tt-GO80qjivBs-DNvSCG74tLsx58Mq7vYXRhSZpIwTjliqv_o4xLKkRdbSg5oSaGlKJrHyYiWG8R64POEestYp0rR5x7Xv25ykPH70wz8PoEtBA03Eaf9M11NgiMKREVE5l4dyJc_vI776JOOb3ROOujM7O2wf9jgF89mcTT</recordid><startdate>20130701</startdate><enddate>20130701</enddate><creator>McKee, Laurel A.K.</creator><creator>Chen, Hao</creator><creator>Regan, Jessica A.</creator><creator>Behunin, Samantha M.</creator><creator>Walker, Jeffery W.</creator><creator>Walker, John S.</creator><creator>Konhilas, John P.</creator><general>Elsevier Inc</general><scope>FBQ</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>7S9</scope><scope>L.6</scope><scope>5PM</scope></search><sort><creationdate>20130701</creationdate><title>Sexually dimorphic myofilament function and cardiac troponin I phosphospecies distribution in hypertrophic cardiomyopathy mice</title><author>McKee, Laurel A.K. ; Chen, Hao ; Regan, Jessica A. ; Behunin, Samantha M. ; Walker, Jeffery W. ; Walker, John S. ; Konhilas, John P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c574t-ba907224b78de9aa1983f7e90502dcd7c9fdd38da18929a52737ac9be3a1bc673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>adenosinetriphosphatase</topic><topic>Animals</topic><topic>Ca2-transporting ATPase</topic><topic>calcium</topic><topic>Calcium - metabolism</topic><topic>cardiomyopathy</topic><topic>Cardiomyopathy, Hypertrophic - enzymology</topic><topic>Cardiomyopathy, Hypertrophic - metabolism</topic><topic>Cardiomyopathy, Hypertrophic - pathology</topic><topic>cTnI</topic><topic>dimorphism</topic><topic>Electrophoresis, Polyacrylamide Gel</topic><topic>Female</topic><topic>females</topic><topic>Heart Ventricles - metabolism</topic><topic>Heart Ventricles - pathology</topic><topic>Hypertrophic cardiomyopathy</topic><topic>Male</topic><topic>males</topic><topic>Mice</topic><topic>Muscle Tonus</topic><topic>mutants</topic><topic>Mutation</topic><topic>Myofibrils - genetics</topic><topic>Myofibrils - metabolism</topic><topic>Myofibrils - physiology</topic><topic>myosin heavy chains</topic><topic>Myosin Heavy Chains - metabolism</topic><topic>Myosin Light Chains - metabolism</topic><topic>Phosphate-affinity SDS–PAGE</topic><topic>Phosphorylation</topic><topic>polyacrylamide gel electrophoresis</topic><topic>post-translational modification</topic><topic>Protein Processing, Post-Translational</topic><topic>Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics</topic><topic>Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism</topic><topic>Sex Factors</topic><topic>Site-specific phosphorylation</topic><topic>SR Ca2+ ATPase (2a) (SERCA2a)</topic><topic>troponin I</topic><topic>Troponin I - metabolism</topic><topic>troponin T</topic><topic>Troponin T - metabolism</topic><topic>Ventricular Myosins - genetics</topic><topic>Ventricular Myosins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McKee, Laurel A.K.</creatorcontrib><creatorcontrib>Chen, Hao</creatorcontrib><creatorcontrib>Regan, Jessica A.</creatorcontrib><creatorcontrib>Behunin, Samantha M.</creatorcontrib><creatorcontrib>Walker, Jeffery W.</creatorcontrib><creatorcontrib>Walker, John S.</creatorcontrib><creatorcontrib>Konhilas, John P.</creatorcontrib><collection>AGRIS</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>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Archives of biochemistry and biophysics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McKee, Laurel A.K.</au><au>Chen, Hao</au><au>Regan, Jessica A.</au><au>Behunin, Samantha M.</au><au>Walker, Jeffery W.</au><au>Walker, John S.</au><au>Konhilas, John P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sexually dimorphic myofilament function and cardiac troponin I phosphospecies distribution in hypertrophic cardiomyopathy mice</atitle><jtitle>Archives of biochemistry and biophysics</jtitle><addtitle>Arch Biochem Biophys</addtitle><date>2013-07-01</date><risdate>2013</risdate><volume>535</volume><issue>1</issue><spage>39</spage><epage>48</epage><pages>39-48</pages><issn>0003-9861</issn><eissn>1096-0384</eissn><abstract>► 10–12Month HCM females develop proportionately larger hearts than HCM males. ► HCM females display alterations in Ca2+-sensitivity over female WT; HCM males do not. ► The pattern of cTnI post-translational modification depends on sex and HCM genotype.
The pathological progression of hypertrophic cardiomyopathy (HCM) is sexually dimorphic such that male HCM mice develop phenotypic indicators of cardiac disease well before female HCM mice. Here, we hypothesized that alterations in myofilament function underlies, in part, this sex dimorphism in HCM disease development. Firstly, 10–12month female HCM (harboring a mutant [R403Q] myosin heavy chain) mice presented with proportionately larger hearts than male HCM mice. Next, we determined Ca2+-sensitive tension development in demembranated cardiac trabeculae excised from 10–12month female and male HCM mice. Whereas HCM did not impact Ca2+-sensitive tension development in male trabeculae, female HCM trabeculae were more sensitive to Ca2+ than wild-type (WT) counterparts and both WT and HCM males. We hypothesized that the underlying cause of this sex difference in Ca2+-sensitive tension development was due to changes in Ca2+ handling and sarcomeric proteins, including expression of SR Ca2+ ATPase (2a) (SERCA2a), β-myosin heavy chain (β-MyHC) and post-translational modifications of myofilament proteins. Female HCM hearts showed an elevation of SERCA2a and β-MyHC protein whereas male HCM hearts showed a similar elevation of β-MyHC protein but a reduced level of cardiac troponin T (cTnT) phosphorylation. We also measured the distribution of cardiac troponin I (cTnI) phosphospecies using phosphate-affinity SDS–PAGE. The distribution of cTnI phosphospecies depended on sex and HCM. In conclusion, female and male HCM mice display sex dimorphic myofilament function that is accompanied by a sex- and HCM-dependent distribution of sarcomeric proteins and cTnI phosphospecies.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>23352598</pmid><doi>10.1016/j.abb.2012.12.023</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | adenosinetriphosphatase Animals Ca2-transporting ATPase calcium Calcium - metabolism cardiomyopathy Cardiomyopathy, Hypertrophic - enzymology Cardiomyopathy, Hypertrophic - metabolism Cardiomyopathy, Hypertrophic - pathology cTnI dimorphism Electrophoresis, Polyacrylamide Gel Female females Heart Ventricles - metabolism Heart Ventricles - pathology Hypertrophic cardiomyopathy Male males Mice Muscle Tonus mutants Mutation Myofibrils - genetics Myofibrils - metabolism Myofibrils - physiology myosin heavy chains Myosin Heavy Chains - metabolism Myosin Light Chains - metabolism Phosphate-affinity SDS–PAGE Phosphorylation polyacrylamide gel electrophoresis post-translational modification Protein Processing, Post-Translational Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism Sex Factors Site-specific phosphorylation SR Ca2+ ATPase (2a) (SERCA2a) troponin I Troponin I - metabolism troponin T Troponin T - metabolism Ventricular Myosins - genetics Ventricular Myosins - metabolism |
| title | Sexually dimorphic myofilament function and cardiac troponin I phosphospecies distribution in hypertrophic cardiomyopathy mice |
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