Alterations of sarcoplasmic reticulum-mediated Ca2+ uptake in a model of premature ventricular contraction (PVC)-induced cardiomyopathy
Premature ventricular contractions (PVCs) are the most frequent ventricular arrhythmias in the overall population. PVCs are known to acutely enhance contractility by the post-extrasystolic potentiation phenomenon, but over time persistent PVCs promote PVC-induced cardiomyopathy (PVC-CM), characteriz...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2023-07, Vol.478 (7), p.1447-1456 |
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| creator | Balderas-Villalobos, Jaime Medina-Contreras, J. M. L. Lynch, Christopher Kabadi, Rajiv Ramirez, Rafael J. Tan, Alex Y. Kaszala, Karoly Samsó, Montserrat Huizar, Jose F. Eltit, Jose M. |
| description | Premature ventricular contractions (PVCs) are the most frequent ventricular arrhythmias in the overall population. PVCs are known to acutely enhance contractility by the post-extrasystolic potentiation phenomenon, but over time persistent PVCs promote PVC-induced cardiomyopathy (PVC-CM), characterized by a reduction of the left ventricular (LV) ejection fraction. Ca
2+
cycling in myocytes commands muscle contraction and in this process, SERCA2 leads the Ca
2+
reuptake into the sarcoplasmic reticulum (SR) shaping cytosolic Ca
2+
signal decay and muscle relaxation. Altered Ca
2+
reuptake can contribute to the contractile dysfunction observed in PVC-CM. To better understand Ca
2+
handling using our PVC-CM model (canines with 50% PVC burden for 12 weeks), SR-Ca
2+
reuptake was investigated by measuring Ca
2+
dynamics and analyzing protein expression. Kinetic analysis of Ca
2+
reuptake in electrically paced myocytes showed a ~ 21 ms delay in PVC-CM compared to Sham in intact isolated myocytes, along with a ~ 13% reduction in SERCA2 activity assessed in permeabilized myocytes. Although these trends were not statistically significant between groups using hierarchical statistics, relaxation of myocytes following contraction was significantly slower in PVC-CM
vs
Sham myocytes. Western blot analyses indicate a 22% reduction in SERCA2 expression, a 23% increase in phospholamban (PLN) expression, and a 50% reduction in PLN phosphorylation in PVC-CM samples
vs
Sham. Computational analysis simulating a 20% decrease in SR-Ca
2+
reuptake resulted in a ~ 22 ms delay in Ca
2+
signal decay, consistent with the experimental result described above. In conclusion, SERCA2 and PLB alterations described above have a modest contribution to functional adaptations observed in PVC-CM. |
| doi_str_mv | 10.1007/s11010-022-04605-y |
| format | Article |
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2+
cycling in myocytes commands muscle contraction and in this process, SERCA2 leads the Ca
2+
reuptake into the sarcoplasmic reticulum (SR) shaping cytosolic Ca
2+
signal decay and muscle relaxation. Altered Ca
2+
reuptake can contribute to the contractile dysfunction observed in PVC-CM. To better understand Ca
2+
handling using our PVC-CM model (canines with 50% PVC burden for 12 weeks), SR-Ca
2+
reuptake was investigated by measuring Ca
2+
dynamics and analyzing protein expression. Kinetic analysis of Ca
2+
reuptake in electrically paced myocytes showed a ~ 21 ms delay in PVC-CM compared to Sham in intact isolated myocytes, along with a ~ 13% reduction in SERCA2 activity assessed in permeabilized myocytes. Although these trends were not statistically significant between groups using hierarchical statistics, relaxation of myocytes following contraction was significantly slower in PVC-CM
vs
Sham myocytes. Western blot analyses indicate a 22% reduction in SERCA2 expression, a 23% increase in phospholamban (PLN) expression, and a 50% reduction in PLN phosphorylation in PVC-CM samples
vs
Sham. Computational analysis simulating a 20% decrease in SR-Ca
2+
reuptake resulted in a ~ 22 ms delay in Ca
2+
signal decay, consistent with the experimental result described above. In conclusion, SERCA2 and PLB alterations described above have a modest contribution to functional adaptations observed in PVC-CM.</description><identifier>ISSN: 0300-8177</identifier><identifier>ISSN: 1573-4919</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-022-04605-y</identifier><identifier>PMID: 36350464</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Biochemistry ; Biomedical and Life Sciences ; Ca2+-transporting ATPase ; Calcium (reticular) ; Calcium influx ; Calcium ions ; Calcium signalling ; Cancer Research ; Cardiology ; Cardiomyopathy ; Decay ; Heart ; Life Sciences ; Medical Biochemistry ; Muscle contraction ; Muscles ; Muscular function ; Myocytes ; Phospholamban ; Phosphorylation ; Reduction ; Sarcoplasmic reticulum ; Statistical analysis ; Ventricle</subject><ispartof>Molecular and cellular biochemistry, 2023-07, Vol.478 (7), p.1447-1456</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c382t-81d3ad62bc904570ec555e4844cbce525548ebb0ba2a769d9bb5ffe3143106473</citedby><cites>FETCH-LOGICAL-c382t-81d3ad62bc904570ec555e4844cbce525548ebb0ba2a769d9bb5ffe3143106473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-022-04605-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-022-04605-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids></links><search><creatorcontrib>Balderas-Villalobos, Jaime</creatorcontrib><creatorcontrib>Medina-Contreras, J. M. L.</creatorcontrib><creatorcontrib>Lynch, Christopher</creatorcontrib><creatorcontrib>Kabadi, Rajiv</creatorcontrib><creatorcontrib>Ramirez, Rafael J.</creatorcontrib><creatorcontrib>Tan, Alex Y.</creatorcontrib><creatorcontrib>Kaszala, Karoly</creatorcontrib><creatorcontrib>Samsó, Montserrat</creatorcontrib><creatorcontrib>Huizar, Jose F.</creatorcontrib><creatorcontrib>Eltit, Jose M.</creatorcontrib><title>Alterations of sarcoplasmic reticulum-mediated Ca2+ uptake in a model of premature ventricular contraction (PVC)-induced cardiomyopathy</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><description>Premature ventricular contractions (PVCs) are the most frequent ventricular arrhythmias in the overall population. PVCs are known to acutely enhance contractility by the post-extrasystolic potentiation phenomenon, but over time persistent PVCs promote PVC-induced cardiomyopathy (PVC-CM), characterized by a reduction of the left ventricular (LV) ejection fraction. Ca
2+
cycling in myocytes commands muscle contraction and in this process, SERCA2 leads the Ca
2+
reuptake into the sarcoplasmic reticulum (SR) shaping cytosolic Ca
2+
signal decay and muscle relaxation. Altered Ca
2+
reuptake can contribute to the contractile dysfunction observed in PVC-CM. To better understand Ca
2+
handling using our PVC-CM model (canines with 50% PVC burden for 12 weeks), SR-Ca
2+
reuptake was investigated by measuring Ca
2+
dynamics and analyzing protein expression. Kinetic analysis of Ca
2+
reuptake in electrically paced myocytes showed a ~ 21 ms delay in PVC-CM compared to Sham in intact isolated myocytes, along with a ~ 13% reduction in SERCA2 activity assessed in permeabilized myocytes. Although these trends were not statistically significant between groups using hierarchical statistics, relaxation of myocytes following contraction was significantly slower in PVC-CM
vs
Sham myocytes. Western blot analyses indicate a 22% reduction in SERCA2 expression, a 23% increase in phospholamban (PLN) expression, and a 50% reduction in PLN phosphorylation in PVC-CM samples
vs
Sham. Computational analysis simulating a 20% decrease in SR-Ca
2+
reuptake resulted in a ~ 22 ms delay in Ca
2+
signal decay, consistent with the experimental result described above. In conclusion, SERCA2 and PLB alterations described above have a modest contribution to functional adaptations observed in PVC-CM.</description><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Ca2+-transporting ATPase</subject><subject>Calcium (reticular)</subject><subject>Calcium influx</subject><subject>Calcium ions</subject><subject>Calcium signalling</subject><subject>Cancer Research</subject><subject>Cardiology</subject><subject>Cardiomyopathy</subject><subject>Decay</subject><subject>Heart</subject><subject>Life Sciences</subject><subject>Medical Biochemistry</subject><subject>Muscle contraction</subject><subject>Muscles</subject><subject>Muscular function</subject><subject>Myocytes</subject><subject>Phospholamban</subject><subject>Phosphorylation</subject><subject>Reduction</subject><subject>Sarcoplasmic reticulum</subject><subject>Statistical analysis</subject><subject>Ventricle</subject><issn>0300-8177</issn><issn>1573-4919</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kU2L1TAUhoMozp3RP-Aq4GZEqvls05UMFx2FAV2o23CanjuTsW1qkg70F_i3Tb2DogtXOZD3eTiHl5BnnL3ijDWvE-eMs4oJUTFVM12tD8iO60ZWquXtQ7JjkrHK8KY5Iacp3bKSZpw_Jieylrogakd-XAwZI2QfpkTDgSaILswDpNE7GjF7twzLWI3Ye8jY0z2Il3SZM3xD6icKdAw9Dhs5RxwhLxHpHU45biBE6kKZwW1-ev7p6_5F5ad-ccXkIPY-jGuYId-sT8ijAwwJn96_Z-TLu7ef9--rq4-XH_YXV5WTRuRyTC-hr0XnWqZ0w9BprVEZpVznUAutlcGuYx0IaOq2b7tOHw4ouZKc1aqRZ-TN0TsvXTnKbavCYOfoR4irDeDt3z-Tv7HX4c4W3GjFeDGc3xti-L5gynb0yeEwwIRhSVY0UtVcCdOW6PN_ordhiVO5zwrDjdbG8E0ojikXQ0oRD7-34cxuRdtj0bYUbX8VbdcCySOUSni6xvhH_R_qJ3sfrPY</recordid><startdate>20230701</startdate><enddate>20230701</enddate><creator>Balderas-Villalobos, Jaime</creator><creator>Medina-Contreras, J. 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M. L.</creatorcontrib><creatorcontrib>Lynch, Christopher</creatorcontrib><creatorcontrib>Kabadi, Rajiv</creatorcontrib><creatorcontrib>Ramirez, Rafael J.</creatorcontrib><creatorcontrib>Tan, Alex Y.</creatorcontrib><creatorcontrib>Kaszala, Karoly</creatorcontrib><creatorcontrib>Samsó, Montserrat</creatorcontrib><creatorcontrib>Huizar, Jose F.</creatorcontrib><creatorcontrib>Eltit, Jose M.</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Balderas-Villalobos, Jaime</au><au>Medina-Contreras, J. M. L.</au><au>Lynch, Christopher</au><au>Kabadi, Rajiv</au><au>Ramirez, Rafael J.</au><au>Tan, Alex Y.</au><au>Kaszala, Karoly</au><au>Samsó, Montserrat</au><au>Huizar, Jose F.</au><au>Eltit, Jose M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alterations of sarcoplasmic reticulum-mediated Ca2+ uptake in a model of premature ventricular contraction (PVC)-induced cardiomyopathy</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><date>2023-07-01</date><risdate>2023</risdate><volume>478</volume><issue>7</issue><spage>1447</spage><epage>1456</epage><pages>1447-1456</pages><issn>0300-8177</issn><issn>1573-4919</issn><eissn>1573-4919</eissn><abstract>Premature ventricular contractions (PVCs) are the most frequent ventricular arrhythmias in the overall population. PVCs are known to acutely enhance contractility by the post-extrasystolic potentiation phenomenon, but over time persistent PVCs promote PVC-induced cardiomyopathy (PVC-CM), characterized by a reduction of the left ventricular (LV) ejection fraction. Ca
2+
cycling in myocytes commands muscle contraction and in this process, SERCA2 leads the Ca
2+
reuptake into the sarcoplasmic reticulum (SR) shaping cytosolic Ca
2+
signal decay and muscle relaxation. Altered Ca
2+
reuptake can contribute to the contractile dysfunction observed in PVC-CM. To better understand Ca
2+
handling using our PVC-CM model (canines with 50% PVC burden for 12 weeks), SR-Ca
2+
reuptake was investigated by measuring Ca
2+
dynamics and analyzing protein expression. Kinetic analysis of Ca
2+
reuptake in electrically paced myocytes showed a ~ 21 ms delay in PVC-CM compared to Sham in intact isolated myocytes, along with a ~ 13% reduction in SERCA2 activity assessed in permeabilized myocytes. Although these trends were not statistically significant between groups using hierarchical statistics, relaxation of myocytes following contraction was significantly slower in PVC-CM
vs
Sham myocytes. Western blot analyses indicate a 22% reduction in SERCA2 expression, a 23% increase in phospholamban (PLN) expression, and a 50% reduction in PLN phosphorylation in PVC-CM samples
vs
Sham. Computational analysis simulating a 20% decrease in SR-Ca
2+
reuptake resulted in a ~ 22 ms delay in Ca
2+
signal decay, consistent with the experimental result described above. In conclusion, SERCA2 and PLB alterations described above have a modest contribution to functional adaptations observed in PVC-CM.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>36350464</pmid><doi>10.1007/s11010-022-04605-y</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Molecular and cellular biochemistry, 2023-07, Vol.478 (7), p.1447-1456 |
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| source | SpringerLink Journals - AutoHoldings |
| subjects | Biochemistry Biomedical and Life Sciences Ca2+-transporting ATPase Calcium (reticular) Calcium influx Calcium ions Calcium signalling Cancer Research Cardiology Cardiomyopathy Decay Heart Life Sciences Medical Biochemistry Muscle contraction Muscles Muscular function Myocytes Phospholamban Phosphorylation Reduction Sarcoplasmic reticulum Statistical analysis Ventricle |
| title | Alterations of sarcoplasmic reticulum-mediated Ca2+ uptake in a model of premature ventricular contraction (PVC)-induced cardiomyopathy |
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