Mechanisms of Ca2+ handling in zebrafish ventricular myocytes
The zebrafish serves as a promising transgenic animal model that can be used to study cardiac Ca 2+ regulation. However, mechanisms of sarcoplasmic reticulum (SR) Ca 2+ handling in the zebrafish heart have not been systematically explored. We found that in zebrafish ventricular myocytes, the action...
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| Veröffentlicht in: | Pflügers Archiv 2013-12, Vol.465 (12), p.1775-1784 |
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| creator | Bovo, Elisa Dvornikov, Alexey V. Mazurek, Stefan R. de Tombe, Pieter P. Zima, Aleksey V. |
| description | The zebrafish serves as a promising transgenic animal model that can be used to study cardiac Ca
2+
regulation. However, mechanisms of sarcoplasmic reticulum (SR) Ca
2+
handling in the zebrafish heart have not been systematically explored. We found that in zebrafish ventricular myocytes, the action potential-induced Ca
2+
transient is mainly (80 %) mediated by Ca
2+
influx via L-type Ca
2+
channels (LTCC) and only 20 % by Ca
2+
released from the SR. This small contribution of the SR to the Ca
2+
transient was not the result of depleted SR Ca
2+
load. We found that the ryanodine receptor (RyR) expression level in zebrafish myocytes was ∼72 % lower compared to rabbit myocytes. In permeabilized myocytes, increasing cytosolic [Ca
2+
] from 100 to 350 nM did not trigger SR Ca
2+
release. However, an application of a low dose of caffeine activated Ca
2+
sparks. These results show that the zebrafish cardiac RyR has low sensitivity to the mechanism of Ca
2+
-induced Ca
2+
release. Activation of protein kinase A by forskolin increased phosphorylation of the RyR in zebrafish myocardium. In half of the studied cells, an increased Ca
2+
transient by forskolin was entirely mediated by augmentation of LTCC current. In the remaining myocytes, the forskolin action was associated with an increase of both LTCC and SR Ca
2+
release. These results indicate that the mechanism of excitation–contraction coupling in zebrafish myocytes differs from the mammalian one mainly because of the small contribution of SR Ca
2+
release to the Ca
2+
transient. This difference is due to a low sensitivity of RyRs to cytosolic [Ca
2+
]. |
| doi_str_mv | 10.1007/s00424-013-1312-2 |
| format | Article |
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2+
regulation. However, mechanisms of sarcoplasmic reticulum (SR) Ca
2+
handling in the zebrafish heart have not been systematically explored. We found that in zebrafish ventricular myocytes, the action potential-induced Ca
2+
transient is mainly (80 %) mediated by Ca
2+
influx via L-type Ca
2+
channels (LTCC) and only 20 % by Ca
2+
released from the SR. This small contribution of the SR to the Ca
2+
transient was not the result of depleted SR Ca
2+
load. We found that the ryanodine receptor (RyR) expression level in zebrafish myocytes was ∼72 % lower compared to rabbit myocytes. In permeabilized myocytes, increasing cytosolic [Ca
2+
] from 100 to 350 nM did not trigger SR Ca
2+
release. However, an application of a low dose of caffeine activated Ca
2+
sparks. These results show that the zebrafish cardiac RyR has low sensitivity to the mechanism of Ca
2+
-induced Ca
2+
release. Activation of protein kinase A by forskolin increased phosphorylation of the RyR in zebrafish myocardium. In half of the studied cells, an increased Ca
2+
transient by forskolin was entirely mediated by augmentation of LTCC current. In the remaining myocytes, the forskolin action was associated with an increase of both LTCC and SR Ca
2+
release. These results indicate that the mechanism of excitation–contraction coupling in zebrafish myocytes differs from the mammalian one mainly because of the small contribution of SR Ca
2+
release to the Ca
2+
transient. This difference is due to a low sensitivity of RyRs to cytosolic [Ca
2+
].</description><identifier>ISSN: 0031-6768</identifier><identifier>EISSN: 1432-2013</identifier><identifier>DOI: 10.1007/s00424-013-1312-2</identifier><identifier>PMID: 23821298</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Biomedical and Life Sciences ; Biomedicine ; Caffeine - pharmacology ; Calcium - metabolism ; Calcium Signaling - physiology ; Cell Biology ; Colforsin - pharmacology ; Cyclic AMP-Dependent Protein Kinases - metabolism ; Excitation Contraction Coupling - drug effects ; Excitation Contraction Coupling - physiology ; Human Physiology ; Molecular Medicine ; Muscle Physiology ; Myocardium - metabolism ; Myocytes, Cardiac - physiology ; Neurosciences ; Rabbits ; Receptors ; Ryanodine Receptor Calcium Release Channel - physiology ; Sarcoplasmic Reticulum - metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism ; Zebrafish</subject><ispartof>Pflügers Archiv, 2013-12, Vol.465 (12), p.1775-1784</ispartof><rights>Springer-Verlag Berlin Heidelberg 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-f50e5ff7cd2c3bce27a72f87c48140eb11a83194de5206264dfcae9fbe7f272f3</citedby><cites>FETCH-LOGICAL-c420t-f50e5ff7cd2c3bce27a72f87c48140eb11a83194de5206264dfcae9fbe7f272f3</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/s00424-013-1312-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00424-013-1312-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23821298$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bovo, Elisa</creatorcontrib><creatorcontrib>Dvornikov, Alexey V.</creatorcontrib><creatorcontrib>Mazurek, Stefan R.</creatorcontrib><creatorcontrib>de Tombe, Pieter P.</creatorcontrib><creatorcontrib>Zima, Aleksey V.</creatorcontrib><title>Mechanisms of Ca2+ handling in zebrafish ventricular myocytes</title><title>Pflügers Archiv</title><addtitle>Pflugers Arch - Eur J Physiol</addtitle><addtitle>Pflugers Arch</addtitle><description>The zebrafish serves as a promising transgenic animal model that can be used to study cardiac Ca
2+
regulation. However, mechanisms of sarcoplasmic reticulum (SR) Ca
2+
handling in the zebrafish heart have not been systematically explored. We found that in zebrafish ventricular myocytes, the action potential-induced Ca
2+
transient is mainly (80 %) mediated by Ca
2+
influx via L-type Ca
2+
channels (LTCC) and only 20 % by Ca
2+
released from the SR. This small contribution of the SR to the Ca
2+
transient was not the result of depleted SR Ca
2+
load. We found that the ryanodine receptor (RyR) expression level in zebrafish myocytes was ∼72 % lower compared to rabbit myocytes. In permeabilized myocytes, increasing cytosolic [Ca
2+
] from 100 to 350 nM did not trigger SR Ca
2+
release. However, an application of a low dose of caffeine activated Ca
2+
sparks. These results show that the zebrafish cardiac RyR has low sensitivity to the mechanism of Ca
2+
-induced Ca
2+
release. Activation of protein kinase A by forskolin increased phosphorylation of the RyR in zebrafish myocardium. In half of the studied cells, an increased Ca
2+
transient by forskolin was entirely mediated by augmentation of LTCC current. In the remaining myocytes, the forskolin action was associated with an increase of both LTCC and SR Ca
2+
release. These results indicate that the mechanism of excitation–contraction coupling in zebrafish myocytes differs from the mammalian one mainly because of the small contribution of SR Ca
2+
release to the Ca
2+
transient. This difference is due to a low sensitivity of RyRs to cytosolic [Ca
2+
].</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Caffeine - pharmacology</subject><subject>Calcium - metabolism</subject><subject>Calcium Signaling - physiology</subject><subject>Cell Biology</subject><subject>Colforsin - pharmacology</subject><subject>Cyclic AMP-Dependent Protein Kinases - metabolism</subject><subject>Excitation Contraction Coupling - drug effects</subject><subject>Excitation Contraction Coupling - physiology</subject><subject>Human Physiology</subject><subject>Molecular Medicine</subject><subject>Muscle Physiology</subject><subject>Myocardium - metabolism</subject><subject>Myocytes, Cardiac - physiology</subject><subject>Neurosciences</subject><subject>Rabbits</subject><subject>Receptors</subject><subject>Ryanodine Receptor Calcium Release Channel - physiology</subject><subject>Sarcoplasmic Reticulum - metabolism</subject><subject>Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism</subject><subject>Zebrafish</subject><issn>0031-6768</issn><issn>1432-2013</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1rGzEQhkVpqV0nPyCXssdC2EYz0lq7hwSCSdtAQi7tWWi1I1tmP1zJG3B-fWXsmOTSkz7mmXeGh7EL4N-Bc3UVOZcocw4iBwGY4wc2BSnSJX19ZFPOBeRzNS8n7EuMa845yhI_swmKEgGrcsquH8muTO9jF7PBZQuDl1l6N63vl5nvsxeqg3E-rrJn6rfB27E1Iet2g91tKZ6xT860kc6P54z9-XH3e_Erf3j6eb-4fcitRL7NXcGpcE7ZBq2oLaEyCl2prCxBcqoBTCmgkg0VyOc4l42zhipXk3KYSDFjN4fczVh31Nj9KqbVm-A7E3Z6MF6_r_R-pZfDs5YgSgUiBXw7BoTh70hxqzsfLbWt6WkYowZZVJWSUGBC4YDaMMQYyJ3GANd77fqgXSfHeq9d73u-vt3v1PHqOQF4AGIq9UsKej2MoU_O_pP6D8efjlg</recordid><startdate>20131201</startdate><enddate>20131201</enddate><creator>Bovo, Elisa</creator><creator>Dvornikov, Alexey V.</creator><creator>Mazurek, Stefan R.</creator><creator>de Tombe, Pieter P.</creator><creator>Zima, Aleksey V.</creator><general>Springer Berlin Heidelberg</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20131201</creationdate><title>Mechanisms of Ca2+ handling in zebrafish ventricular myocytes</title><author>Bovo, Elisa ; Dvornikov, Alexey V. ; Mazurek, Stefan R. ; de Tombe, Pieter P. ; Zima, Aleksey V.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-f50e5ff7cd2c3bce27a72f87c48140eb11a83194de5206264dfcae9fbe7f272f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Caffeine - pharmacology</topic><topic>Calcium - metabolism</topic><topic>Calcium Signaling - physiology</topic><topic>Cell Biology</topic><topic>Colforsin - pharmacology</topic><topic>Cyclic AMP-Dependent Protein Kinases - metabolism</topic><topic>Excitation Contraction Coupling - drug effects</topic><topic>Excitation Contraction Coupling - physiology</topic><topic>Human Physiology</topic><topic>Molecular Medicine</topic><topic>Muscle Physiology</topic><topic>Myocardium - metabolism</topic><topic>Myocytes, Cardiac - physiology</topic><topic>Neurosciences</topic><topic>Rabbits</topic><topic>Receptors</topic><topic>Ryanodine Receptor Calcium Release Channel - physiology</topic><topic>Sarcoplasmic Reticulum - metabolism</topic><topic>Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism</topic><topic>Zebrafish</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bovo, Elisa</creatorcontrib><creatorcontrib>Dvornikov, Alexey V.</creatorcontrib><creatorcontrib>Mazurek, Stefan R.</creatorcontrib><creatorcontrib>de Tombe, Pieter P.</creatorcontrib><creatorcontrib>Zima, Aleksey V.</creatorcontrib><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>PubMed Central (Full Participant titles)</collection><jtitle>Pflügers Archiv</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bovo, Elisa</au><au>Dvornikov, Alexey V.</au><au>Mazurek, Stefan R.</au><au>de Tombe, Pieter P.</au><au>Zima, Aleksey V.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanisms of Ca2+ handling in zebrafish ventricular myocytes</atitle><jtitle>Pflügers Archiv</jtitle><stitle>Pflugers Arch - Eur J Physiol</stitle><addtitle>Pflugers Arch</addtitle><date>2013-12-01</date><risdate>2013</risdate><volume>465</volume><issue>12</issue><spage>1775</spage><epage>1784</epage><pages>1775-1784</pages><issn>0031-6768</issn><eissn>1432-2013</eissn><abstract>The zebrafish serves as a promising transgenic animal model that can be used to study cardiac Ca
2+
regulation. However, mechanisms of sarcoplasmic reticulum (SR) Ca
2+
handling in the zebrafish heart have not been systematically explored. We found that in zebrafish ventricular myocytes, the action potential-induced Ca
2+
transient is mainly (80 %) mediated by Ca
2+
influx via L-type Ca
2+
channels (LTCC) and only 20 % by Ca
2+
released from the SR. This small contribution of the SR to the Ca
2+
transient was not the result of depleted SR Ca
2+
load. We found that the ryanodine receptor (RyR) expression level in zebrafish myocytes was ∼72 % lower compared to rabbit myocytes. In permeabilized myocytes, increasing cytosolic [Ca
2+
] from 100 to 350 nM did not trigger SR Ca
2+
release. However, an application of a low dose of caffeine activated Ca
2+
sparks. These results show that the zebrafish cardiac RyR has low sensitivity to the mechanism of Ca
2+
-induced Ca
2+
release. Activation of protein kinase A by forskolin increased phosphorylation of the RyR in zebrafish myocardium. In half of the studied cells, an increased Ca
2+
transient by forskolin was entirely mediated by augmentation of LTCC current. In the remaining myocytes, the forskolin action was associated with an increase of both LTCC and SR Ca
2+
release. These results indicate that the mechanism of excitation–contraction coupling in zebrafish myocytes differs from the mammalian one mainly because of the small contribution of SR Ca
2+
release to the Ca
2+
transient. This difference is due to a low sensitivity of RyRs to cytosolic [Ca
2+
].</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>23821298</pmid><doi>10.1007/s00424-013-1312-2</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| language | eng |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Animals Biomedical and Life Sciences Biomedicine Caffeine - pharmacology Calcium - metabolism Calcium Signaling - physiology Cell Biology Colforsin - pharmacology Cyclic AMP-Dependent Protein Kinases - metabolism Excitation Contraction Coupling - drug effects Excitation Contraction Coupling - physiology Human Physiology Molecular Medicine Muscle Physiology Myocardium - metabolism Myocytes, Cardiac - physiology Neurosciences Rabbits Receptors Ryanodine Receptor Calcium Release Channel - physiology Sarcoplasmic Reticulum - metabolism Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism Zebrafish |
| title | Mechanisms of Ca2+ handling in zebrafish ventricular myocytes |
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