Mitochondrial Deformation During the Cardiac Mechanical Cycle
ABSTRACT Cardiomyocytes both cause and experience continual cyclic deformation. The exact effects of this deformation on the properties of intracellular organelles are not well characterized, although they are likely to be relevant for cardiomyocyte responses to active and passive changes in their m...
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Veröffentlicht in: | Anatomical record (Hoboken, N.J. : 2007) N.J. : 2007), 2019-01, Vol.302 (1), p.146-152 |
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creator | Rog‐Zielinska, E. A. O'Toole, E. T. Hoenger, A. Kohl, P. |
description | ABSTRACT
Cardiomyocytes both cause and experience continual cyclic deformation. The exact effects of this deformation on the properties of intracellular organelles are not well characterized, although they are likely to be relevant for cardiomyocyte responses to active and passive changes in their mechanical environment. In the present study we provide three‐dimensional ultrastructural evidence for mechanically induced mitochondrial deformation in rabbit ventricular cardiomyocytes over a range of sarcomere lengths representing myocardial tissue stretch, an unloaded “slack” state, and contracture. We also show structural indications for interaction of mitochondria with one another, as well as with other intracellular elements such as microtubules, sarcoplasmic reticulum and T‐tubules. The data presented here help to contextualize recent reports on the mechanosensitivity and cell‐wide connectivity of the mitochondrial network and provide a structural framework that may aide interpretation of mechanically‐regulated molecular signaling in cardiac cells. Anat Rec, 302:146–152, 2019. © 2018 The Authors. The Anatomical Record published by Wiley Periodicals, Inc. on behalf of American Association of Anatomists. |
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Cardiomyocytes both cause and experience continual cyclic deformation. The exact effects of this deformation on the properties of intracellular organelles are not well characterized, although they are likely to be relevant for cardiomyocyte responses to active and passive changes in their mechanical environment. In the present study we provide three‐dimensional ultrastructural evidence for mechanically induced mitochondrial deformation in rabbit ventricular cardiomyocytes over a range of sarcomere lengths representing myocardial tissue stretch, an unloaded “slack” state, and contracture. We also show structural indications for interaction of mitochondria with one another, as well as with other intracellular elements such as microtubules, sarcoplasmic reticulum and T‐tubules. The data presented here help to contextualize recent reports on the mechanosensitivity and cell‐wide connectivity of the mitochondrial network and provide a structural framework that may aide interpretation of mechanically‐regulated molecular signaling in cardiac cells. Anat Rec, 302:146–152, 2019. © 2018 The Authors. The Anatomical Record published by Wiley Periodicals, Inc. on behalf of American Association of Anatomists.</description><identifier>ISSN: 1932-8486</identifier><identifier>EISSN: 1932-8494</identifier><identifier>DOI: 10.1002/ar.23917</identifier><identifier>PMID: 30302911</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>Actin Cytoskeleton ; Animals ; Cardiac muscle ; Cardiomyocytes ; electron tomography ; Full Length Special Issue ; Heart ; Heart Ventricles - pathology ; Intracellular ; mechanosensitivity ; Microtubules ; Microtubules - pathology ; Mitochondria ; Mitochondria - pathology ; Myocytes, Cardiac - pathology ; Organelles ; Rabbits ; Sarcomeres - pathology ; Sarcoplasmic reticulum ; Sarcoplasmic Reticulum - pathology ; Special Issue ; Stress, Mechanical ; Tubules ; Ventricle</subject><ispartof>Anatomical record (Hoboken, N.J. : 2007), 2019-01, Vol.302 (1), p.146-152</ispartof><rights>2018 The Authors. published by Wiley Periodicals, Inc. on behalf of American Association of Anatomists.</rights><rights>2018 The Authors. The Anatomical Record published by Wiley Periodicals, Inc. on behalf of American Association of Anatomists.</rights><rights>2019 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5047-3c173885d63170f54f15b1ccdec9019bfd661c48dceb3b775042b3762ccaf89e3</citedby><cites>FETCH-LOGICAL-c5047-3c173885d63170f54f15b1ccdec9019bfd661c48dceb3b775042b3762ccaf89e3</cites><orcidid>0000-0002-3295-4728</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Far.23917$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Far.23917$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,1417,1433,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30302911$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rog‐Zielinska, E. A.</creatorcontrib><creatorcontrib>O'Toole, E. T.</creatorcontrib><creatorcontrib>Hoenger, A.</creatorcontrib><creatorcontrib>Kohl, P.</creatorcontrib><title>Mitochondrial Deformation During the Cardiac Mechanical Cycle</title><title>Anatomical record (Hoboken, N.J. : 2007)</title><addtitle>Anat Rec (Hoboken)</addtitle><description>ABSTRACT
Cardiomyocytes both cause and experience continual cyclic deformation. The exact effects of this deformation on the properties of intracellular organelles are not well characterized, although they are likely to be relevant for cardiomyocyte responses to active and passive changes in their mechanical environment. In the present study we provide three‐dimensional ultrastructural evidence for mechanically induced mitochondrial deformation in rabbit ventricular cardiomyocytes over a range of sarcomere lengths representing myocardial tissue stretch, an unloaded “slack” state, and contracture. We also show structural indications for interaction of mitochondria with one another, as well as with other intracellular elements such as microtubules, sarcoplasmic reticulum and T‐tubules. The data presented here help to contextualize recent reports on the mechanosensitivity and cell‐wide connectivity of the mitochondrial network and provide a structural framework that may aide interpretation of mechanically‐regulated molecular signaling in cardiac cells. Anat Rec, 302:146–152, 2019. © 2018 The Authors. The Anatomical Record published by Wiley Periodicals, Inc. on behalf of American Association of Anatomists.</description><subject>Actin Cytoskeleton</subject><subject>Animals</subject><subject>Cardiac muscle</subject><subject>Cardiomyocytes</subject><subject>electron tomography</subject><subject>Full Length Special Issue</subject><subject>Heart</subject><subject>Heart Ventricles - pathology</subject><subject>Intracellular</subject><subject>mechanosensitivity</subject><subject>Microtubules</subject><subject>Microtubules - pathology</subject><subject>Mitochondria</subject><subject>Mitochondria - pathology</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Organelles</subject><subject>Rabbits</subject><subject>Sarcomeres - pathology</subject><subject>Sarcoplasmic reticulum</subject><subject>Sarcoplasmic Reticulum - pathology</subject><subject>Special Issue</subject><subject>Stress, Mechanical</subject><subject>Tubules</subject><subject>Ventricle</subject><issn>1932-8486</issn><issn>1932-8494</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><recordid>eNp1kVtLwzAYhoMobh7AXyAFb7zpzKFNmguF0XmCDUH0OqRpuma0zUxbZf_e6OY8gFdf4Hvy5A0vACcIjhCE-EK6ESYcsR0wRJzgMIl4tLs9J3QADtp2AWEcQU72wYBAAjFHaAguZ6azqrRN7oysgokurKtlZ2wTTHpnmnnQlTpIpcuNVMFMq1I2RnkyXalKH4G9QlatPt7MQ_B8c_2U3oXTh9v7dDwNVQwjFhKFGEmSOKcEMVjEUYHiDCmVa8Uh4lmRU4pUlORKZyRjzF_CGWEUKyWLhGtyCK7W3mWf1dpjTedkJZbO1NKthJVG_N40phRz-yr8gzji1AvONwJnX3rddqI2rdJVJRtt-1ZghFiCYUyJR8_-oAvbu8Z_z1MUMcogx99C5WzbOl1swyAoPjoR0onPTjx6-jP8FvwqwQPhGngzlV79KxLjx7XwHfqglBQ</recordid><startdate>201901</startdate><enddate>201901</enddate><creator>Rog‐Zielinska, E. A.</creator><creator>O'Toole, E. T.</creator><creator>Hoenger, A.</creator><creator>Kohl, P.</creator><general>John Wiley & Sons, Inc</general><general>Wiley Subscription Services, Inc</general><scope>24P</scope><scope>WIN</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>7QR</scope><scope>7TK</scope><scope>7TS</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3295-4728</orcidid></search><sort><creationdate>201901</creationdate><title>Mitochondrial Deformation During the Cardiac Mechanical Cycle</title><author>Rog‐Zielinska, E. A. ; O'Toole, E. T. ; Hoenger, A. ; Kohl, P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5047-3c173885d63170f54f15b1ccdec9019bfd661c48dceb3b775042b3762ccaf89e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Actin Cytoskeleton</topic><topic>Animals</topic><topic>Cardiac muscle</topic><topic>Cardiomyocytes</topic><topic>electron tomography</topic><topic>Full Length Special Issue</topic><topic>Heart</topic><topic>Heart Ventricles - pathology</topic><topic>Intracellular</topic><topic>mechanosensitivity</topic><topic>Microtubules</topic><topic>Microtubules - pathology</topic><topic>Mitochondria</topic><topic>Mitochondria - pathology</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Organelles</topic><topic>Rabbits</topic><topic>Sarcomeres - pathology</topic><topic>Sarcoplasmic reticulum</topic><topic>Sarcoplasmic Reticulum - pathology</topic><topic>Special Issue</topic><topic>Stress, Mechanical</topic><topic>Tubules</topic><topic>Ventricle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rog‐Zielinska, E. A.</creatorcontrib><creatorcontrib>O'Toole, E. T.</creatorcontrib><creatorcontrib>Hoenger, A.</creatorcontrib><creatorcontrib>Kohl, P.</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Wiley Online Library (Open Access Collection)</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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Anatomical record (Hoboken, N.J. : 2007)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rog‐Zielinska, E. 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Cardiomyocytes both cause and experience continual cyclic deformation. The exact effects of this deformation on the properties of intracellular organelles are not well characterized, although they are likely to be relevant for cardiomyocyte responses to active and passive changes in their mechanical environment. In the present study we provide three‐dimensional ultrastructural evidence for mechanically induced mitochondrial deformation in rabbit ventricular cardiomyocytes over a range of sarcomere lengths representing myocardial tissue stretch, an unloaded “slack” state, and contracture. We also show structural indications for interaction of mitochondria with one another, as well as with other intracellular elements such as microtubules, sarcoplasmic reticulum and T‐tubules. The data presented here help to contextualize recent reports on the mechanosensitivity and cell‐wide connectivity of the mitochondrial network and provide a structural framework that may aide interpretation of mechanically‐regulated molecular signaling in cardiac cells. Anat Rec, 302:146–152, 2019. © 2018 The Authors. The Anatomical Record published by Wiley Periodicals, Inc. on behalf of American Association of Anatomists.</abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>30302911</pmid><doi>10.1002/ar.23917</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0002-3295-4728</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Actin Cytoskeleton Animals Cardiac muscle Cardiomyocytes electron tomography Full Length Special Issue Heart Heart Ventricles - pathology Intracellular mechanosensitivity Microtubules Microtubules - pathology Mitochondria Mitochondria - pathology Myocytes, Cardiac - pathology Organelles Rabbits Sarcomeres - pathology Sarcoplasmic reticulum Sarcoplasmic Reticulum - pathology Special Issue Stress, Mechanical Tubules Ventricle |
title | Mitochondrial Deformation During the Cardiac Mechanical Cycle |
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