Rapid changes in cardiac myofilament function following the acute activation of estrogen receptor-alpha
Estrogens have well-recognized and complex cardiovascular effects, including altering myocardial contractility through changes in myofilament function. The presence of multiple estrogen receptor (ER) isoforms in the heart may explain some discrepant findings about the cardiac effects of estrogens. M...
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| description | Estrogens have well-recognized and complex cardiovascular effects, including altering myocardial contractility through changes in myofilament function. The presence of multiple estrogen receptor (ER) isoforms in the heart may explain some discrepant findings about the cardiac effects of estrogens. Most studies examining the impact of estrogens on the heart have focused on chronic changes in estrogen levels, and have not investigated rapid, non-genomic pathways. The first objective of this study was to determine how acute activation of ERα impacts cardiac myofilaments. Nongenomic myocardial estrogen signaling is associated with the activation of a variety of signaling pathways. p38 MAPK has been implicated in acute ER signaling in the heart, and is known to affect myofilament function. Thus, the second objective of this study was to determine if acute ERα activation mediates its myofilament effects through p38 MAPK recruitment. Hearts from female C57Bl/6 mice were perfused with the ERα agonist PPT and myofilaments isolated. Activation of ERα depressed actomyosin MgATPase activity and decreased myofilament calcium sensitivity. Inhibition of p38 MAPK attenuated the myofilament effects of ERα activation. ERα stimulation did not affect global myofilament protein phosphorylation, but troponin I phosphorylation at the putative PKA phosphorylation sites was decreased. Changes in myofilament activation did not translate into alterations in whole heart function. The present study provides evidence supporting rapid, non-genomic changes in cardiac myofilament function following acute ERα stimulation mediated by the p38 MAPK pathway. |
| doi_str_mv | 10.1371/journal.pone.0041076 |
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The presence of multiple estrogen receptor (ER) isoforms in the heart may explain some discrepant findings about the cardiac effects of estrogens. Most studies examining the impact of estrogens on the heart have focused on chronic changes in estrogen levels, and have not investigated rapid, non-genomic pathways. The first objective of this study was to determine how acute activation of ERα impacts cardiac myofilaments. Nongenomic myocardial estrogen signaling is associated with the activation of a variety of signaling pathways. p38 MAPK has been implicated in acute ER signaling in the heart, and is known to affect myofilament function. Thus, the second objective of this study was to determine if acute ERα activation mediates its myofilament effects through p38 MAPK recruitment. Hearts from female C57Bl/6 mice were perfused with the ERα agonist PPT and myofilaments isolated. Activation of ERα depressed actomyosin MgATPase activity and decreased myofilament calcium sensitivity. Inhibition of p38 MAPK attenuated the myofilament effects of ERα activation. ERα stimulation did not affect global myofilament protein phosphorylation, but troponin I phosphorylation at the putative PKA phosphorylation sites was decreased. Changes in myofilament activation did not translate into alterations in whole heart function. The present study provides evidence supporting rapid, non-genomic changes in cardiac myofilament function following acute ERα stimulation mediated by the p38 MAPK pathway.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0041076</identifier><identifier>PMID: 22859967</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Activation ; Actomyosin ; Animals ; Biology ; Calcium ; Calcium-binding protein ; Estrogen Receptor alpha - metabolism ; Estrogen Receptor alpha - physiology ; Estrogen receptors ; Estrogens ; Estrogens - pharmacology ; Female ; Heart ; Heart diseases ; Heart function ; Heart Ventricles - cytology ; Hormone replacement therapy ; Imidazoles - pharmacology ; In Vitro Techniques ; Isoforms ; Kinases ; MAP kinase ; Medicine ; Mice ; Mice, Inbred C57BL ; Muscle contraction ; Muscle Proteins - metabolism ; Myofibrils - drug effects ; Myofibrils - metabolism ; Myofibrils - physiology ; p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases - metabolism ; Phenols (Class of compounds) ; Phenols - pharmacology ; Phosphorylation ; Protein kinase A ; Protein Processing, Post-Translational ; Pyrazoles - pharmacology ; Pyridines - pharmacology ; Rodents ; Signal transduction ; Signaling ; Stimulation ; Troponin ; Troponin I ; Troponin I - metabolism ; Ventricular Function, Left - drug effects ; Ventricular Pressure - drug effects</subject><ispartof>PloS one, 2012-07, Vol.7 (7), p.e41076-e41076</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>Kulpa et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2012 Kulpa et al 2012 Kulpa et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-940700b2356c67213c0a3743b2dbf2f30b595d6e8c7c6da1acc94195d225e0193</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408454/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408454/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,2098,2917,23849,27907,27908,53774,53776,79351,79352</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22859967$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Wold, Loren E.</contributor><creatorcontrib>Kulpa, Justyna</creatorcontrib><creatorcontrib>Chinnappareddy, Nirmala</creatorcontrib><creatorcontrib>Pyle, W Glen</creatorcontrib><title>Rapid changes in cardiac myofilament function following the acute activation of estrogen receptor-alpha</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Estrogens have well-recognized and complex cardiovascular effects, including altering myocardial contractility through changes in myofilament function. The presence of multiple estrogen receptor (ER) isoforms in the heart may explain some discrepant findings about the cardiac effects of estrogens. Most studies examining the impact of estrogens on the heart have focused on chronic changes in estrogen levels, and have not investigated rapid, non-genomic pathways. The first objective of this study was to determine how acute activation of ERα impacts cardiac myofilaments. Nongenomic myocardial estrogen signaling is associated with the activation of a variety of signaling pathways. p38 MAPK has been implicated in acute ER signaling in the heart, and is known to affect myofilament function. Thus, the second objective of this study was to determine if acute ERα activation mediates its myofilament effects through p38 MAPK recruitment. Hearts from female C57Bl/6 mice were perfused with the ERα agonist PPT and myofilaments isolated. Activation of ERα depressed actomyosin MgATPase activity and decreased myofilament calcium sensitivity. Inhibition of p38 MAPK attenuated the myofilament effects of ERα activation. ERα stimulation did not affect global myofilament protein phosphorylation, but troponin I phosphorylation at the putative PKA phosphorylation sites was decreased. Changes in myofilament activation did not translate into alterations in whole heart function. The present study provides evidence supporting rapid, non-genomic changes in cardiac myofilament function following acute ERα stimulation mediated by the p38 MAPK pathway.</description><subject>Activation</subject><subject>Actomyosin</subject><subject>Animals</subject><subject>Biology</subject><subject>Calcium</subject><subject>Calcium-binding protein</subject><subject>Estrogen Receptor alpha - metabolism</subject><subject>Estrogen Receptor alpha - physiology</subject><subject>Estrogen receptors</subject><subject>Estrogens</subject><subject>Estrogens - pharmacology</subject><subject>Female</subject><subject>Heart</subject><subject>Heart diseases</subject><subject>Heart function</subject><subject>Heart Ventricles - cytology</subject><subject>Hormone replacement therapy</subject><subject>Imidazoles - pharmacology</subject><subject>In Vitro Techniques</subject><subject>Isoforms</subject><subject>Kinases</subject><subject>MAP kinase</subject><subject>Medicine</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Muscle contraction</subject><subject>Muscle Proteins - metabolism</subject><subject>Myofibrils - drug effects</subject><subject>Myofibrils - metabolism</subject><subject>Myofibrils - physiology</subject><subject>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Phenols (Class of compounds)</subject><subject>Phenols - pharmacology</subject><subject>Phosphorylation</subject><subject>Protein kinase A</subject><subject>Protein Processing, Post-Translational</subject><subject>Pyrazoles - pharmacology</subject><subject>Pyridines - pharmacology</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Stimulation</subject><subject>Troponin</subject><subject>Troponin I</subject><subject>Troponin I - metabolism</subject><subject>Ventricular Function, Left - drug effects</subject><subject>Ventricular Pressure - drug effects</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk21r1TAUx4sobk6_gWhBEH1xr3lq2r4RxvDhwmAwH96G0zRtM9KmJul03950txu3shdS0jbJ7_yT809OkrzEaItpjj9c2ckNYLajHdQWIYZRzh8lx7ikZMMJoo8P_o-SZ95fIZTRgvOnyREhRVaWPD9O2ksYdZ3KDoZW-VQPqQRXa5Bpf2MbbaBXQ0ibaZBB2yFtrDH2tx7aNHQqBTmF-R30NdxO2yZVPjjbqiF1SqoxWLcBM3bwPHnSgPHqxfI9SX58_vT97Ovm_OLL7uz0fCN5ScKmZChHqCI045LnBFOJgOaMVqSuGtJQVGVlVnNVyFzyGjBIWTIchwjJFIr5niSv97qjsV4sHnmBKckYn1skdnuitnAlRqd7cDfCgha3A9a1AlzQ0igBtCZQAuRNkbM6i1vBOaoVw7whsVNFrY_LalPVq1pGrxyYleh6ZtCdaO21oAwVLGNR4N0i4OyvKXoneu2lMgYGZae4b0QxzoqCzZm9-Qd9OLuFaiEmoIfGxnXlLCpOWVkQRouiiNT2ASo-teq1jBcqnrxaB7xfBUQmqD-hhcl7sft2-f_sxc81-_aA7RSY0Hlrpvk2-TXI9qB01nunmnuTMRJzPdy5IeZ6EEs9xLBXhwd0H3RXAPQvyhEF9A</recordid><startdate>20120730</startdate><enddate>20120730</enddate><creator>Kulpa, Justyna</creator><creator>Chinnappareddy, Nirmala</creator><creator>Pyle, W Glen</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120730</creationdate><title>Rapid changes in cardiac myofilament function following the acute activation of estrogen receptor-alpha</title><author>Kulpa, Justyna ; Chinnappareddy, Nirmala ; Pyle, W Glen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-940700b2356c67213c0a3743b2dbf2f30b595d6e8c7c6da1acc94195d225e0193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Activation</topic><topic>Actomyosin</topic><topic>Animals</topic><topic>Biology</topic><topic>Calcium</topic><topic>Calcium-binding protein</topic><topic>Estrogen Receptor alpha - metabolism</topic><topic>Estrogen Receptor alpha - physiology</topic><topic>Estrogen receptors</topic><topic>Estrogens</topic><topic>Estrogens - pharmacology</topic><topic>Female</topic><topic>Heart</topic><topic>Heart diseases</topic><topic>Heart function</topic><topic>Heart Ventricles - cytology</topic><topic>Hormone replacement therapy</topic><topic>Imidazoles - pharmacology</topic><topic>In Vitro Techniques</topic><topic>Isoforms</topic><topic>Kinases</topic><topic>MAP kinase</topic><topic>Medicine</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Muscle contraction</topic><topic>Muscle Proteins - metabolism</topic><topic>Myofibrils - drug effects</topic><topic>Myofibrils - metabolism</topic><topic>Myofibrils - physiology</topic><topic>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Phenols (Class of compounds)</topic><topic>Phenols - pharmacology</topic><topic>Phosphorylation</topic><topic>Protein kinase A</topic><topic>Protein Processing, Post-Translational</topic><topic>Pyrazoles - pharmacology</topic><topic>Pyridines - pharmacology</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Stimulation</topic><topic>Troponin</topic><topic>Troponin I</topic><topic>Troponin I - metabolism</topic><topic>Ventricular Function, Left - drug effects</topic><topic>Ventricular Pressure - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kulpa, Justyna</creatorcontrib><creatorcontrib>Chinnappareddy, Nirmala</creatorcontrib><creatorcontrib>Pyle, W Glen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</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>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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The presence of multiple estrogen receptor (ER) isoforms in the heart may explain some discrepant findings about the cardiac effects of estrogens. Most studies examining the impact of estrogens on the heart have focused on chronic changes in estrogen levels, and have not investigated rapid, non-genomic pathways. The first objective of this study was to determine how acute activation of ERα impacts cardiac myofilaments. Nongenomic myocardial estrogen signaling is associated with the activation of a variety of signaling pathways. p38 MAPK has been implicated in acute ER signaling in the heart, and is known to affect myofilament function. Thus, the second objective of this study was to determine if acute ERα activation mediates its myofilament effects through p38 MAPK recruitment. Hearts from female C57Bl/6 mice were perfused with the ERα agonist PPT and myofilaments isolated. Activation of ERα depressed actomyosin MgATPase activity and decreased myofilament calcium sensitivity. Inhibition of p38 MAPK attenuated the myofilament effects of ERα activation. ERα stimulation did not affect global myofilament protein phosphorylation, but troponin I phosphorylation at the putative PKA phosphorylation sites was decreased. Changes in myofilament activation did not translate into alterations in whole heart function. The present study provides evidence supporting rapid, non-genomic changes in cardiac myofilament function following acute ERα stimulation mediated by the p38 MAPK pathway.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22859967</pmid><doi>10.1371/journal.pone.0041076</doi><tpages>e41076</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Activation Actomyosin Animals Biology Calcium Calcium-binding protein Estrogen Receptor alpha - metabolism Estrogen Receptor alpha - physiology Estrogen receptors Estrogens Estrogens - pharmacology Female Heart Heart diseases Heart function Heart Ventricles - cytology Hormone replacement therapy Imidazoles - pharmacology In Vitro Techniques Isoforms Kinases MAP kinase Medicine Mice Mice, Inbred C57BL Muscle contraction Muscle Proteins - metabolism Myofibrils - drug effects Myofibrils - metabolism Myofibrils - physiology p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors p38 Mitogen-Activated Protein Kinases - metabolism Phenols (Class of compounds) Phenols - pharmacology Phosphorylation Protein kinase A Protein Processing, Post-Translational Pyrazoles - pharmacology Pyridines - pharmacology Rodents Signal transduction Signaling Stimulation Troponin Troponin I Troponin I - metabolism Ventricular Function, Left - drug effects Ventricular Pressure - drug effects |
| title | Rapid changes in cardiac myofilament function following the acute activation of estrogen receptor-alpha |
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