Measuring tendon properties in mdx mice: Cell viability and viscoelastic characteristics
Abstract Muscular dystrophy is a genetic disorder of skeletal muscle characterized by progressive muscle weakness. Here we assessed whether muscle wasting affects cell viability and mechanical properties of extensor digitorum longus (EDL) and of tibialis anterior (TA) tendons from mdx dystrophic mic...
Gespeichert in:
Veröffentlicht in: | Journal of biomechanics 2009-10, Vol.42 (14), p.2243-2248 |
---|---|
Hauptverfasser: | , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 2248 |
---|---|
container_issue | 14 |
container_start_page | 2243 |
container_title | Journal of biomechanics |
container_volume | 42 |
creator | Rizzuto, E Musarò, A Catizone, A Del Prete, Z |
description | Abstract Muscular dystrophy is a genetic disorder of skeletal muscle characterized by progressive muscle weakness. Here we assessed whether muscle wasting affects cell viability and mechanical properties of extensor digitorum longus (EDL) and of tibialis anterior (TA) tendons from mdx dystrophic mice compared to wild type (WT) mice. mdx mice represent the classical animal model for human Duchenne muscular dystrophy, and show several signs of the pathology, including a decrease in specific force and an increase of fibrotic index. Cell viability of tendons was evaluated by histological analysis, and viscoelastic properties have been assessed by a rapid measurement protocol that allowed us to compute, at the same time, tissue complex compliance for all the frequencies of interest. Confocal microscopy and mechanical properties measurements revealed that mdx tendons, compared to WT ones, have an increase in the number of dead cells and a significant reduction in tissue elasticity for all the frequencies that were tested. These findings indicate a reduced quality of the tissue. Moreover, mdx tendons have an increase in the viscous response, indicating that during dynamic loading, they dissipate more energy compared to WT. Our results demonstrate that muscular dystrophy involves not only muscle wasting, but also alteration in the viscoelastic properties of tendons, suggesting a paracrine effect of altered skeletal muscle on tendinous tissue. |
doi_str_mv | 10.1016/j.jbiomech.2009.06.041 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_734070774</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>1_s2_0_S0021929009003856</els_id><sourcerecordid>2744239331</sourcerecordid><originalsourceid>FETCH-LOGICAL-c481t-2386472f1a64d5e526e185460d69074f6cc3f7f01bd9e87307c1a87b0547eafa3</originalsourceid><addsrcrecordid>eNqFkk-LFDEQxYMo7uzqV1gCgp6mrXTSSdqDKIOrwooHFbyFdFLtpu0_Y9K9ON_eNDOysAeFQCj4VeW9vCLkkkHBgMmXXdE1YRrQ3RQlQF2ALECwB2TDtOLbkmt4SDYAJdvWZQ1n5DylDgCUUPVjcsZqKSvG-YZ8_4Q2LTGMP-iMo59Guo_THuMcMNEw0sH_pkNw-IrusO_pbbBN6MN8oHb0uUpuwt6mOTjqbmy0bsYY1jI9IY9a2yd8erovyLerd193H7bXn99_3L293jqh2bwqlUKVLbNS-AqrUiLTlZDgZZ3VttI53qoWWONrzNZAOWa1aqASCm1r-QV5cZybdf9aMM1myKqyVjvitCSjuAAFSolMPv8nyYXWutKQwWf3wG5a4phdGAZc1EJXUmZKHikXp5QitmYfw2DjIUNmzch05m9GZs3IgDQ5o9x4eRq_NAP6u7ZTKBl4cwQw_9ttwGiSCzg69CGim42fwv_feH1vhOvDGJztf-IB050fk0oD5su6KeuiQD482-N_AK_huhU</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1034948566</pqid></control><display><type>article</type><title>Measuring tendon properties in mdx mice: Cell viability and viscoelastic characteristics</title><source>MEDLINE</source><source>ScienceDirect Journals (5 years ago - present)</source><source>ProQuest Central UK/Ireland</source><creator>Rizzuto, E ; Musarò, A ; Catizone, A ; Del Prete, Z</creator><creatorcontrib>Rizzuto, E ; Musarò, A ; Catizone, A ; Del Prete, Z</creatorcontrib><description>Abstract Muscular dystrophy is a genetic disorder of skeletal muscle characterized by progressive muscle weakness. Here we assessed whether muscle wasting affects cell viability and mechanical properties of extensor digitorum longus (EDL) and of tibialis anterior (TA) tendons from mdx dystrophic mice compared to wild type (WT) mice. mdx mice represent the classical animal model for human Duchenne muscular dystrophy, and show several signs of the pathology, including a decrease in specific force and an increase of fibrotic index. Cell viability of tendons was evaluated by histological analysis, and viscoelastic properties have been assessed by a rapid measurement protocol that allowed us to compute, at the same time, tissue complex compliance for all the frequencies of interest. Confocal microscopy and mechanical properties measurements revealed that mdx tendons, compared to WT ones, have an increase in the number of dead cells and a significant reduction in tissue elasticity for all the frequencies that were tested. These findings indicate a reduced quality of the tissue. Moreover, mdx tendons have an increase in the viscous response, indicating that during dynamic loading, they dissipate more energy compared to WT. Our results demonstrate that muscular dystrophy involves not only muscle wasting, but also alteration in the viscoelastic properties of tendons, suggesting a paracrine effect of altered skeletal muscle on tendinous tissue.</description><identifier>ISSN: 0021-9290</identifier><identifier>EISSN: 1873-2380</identifier><identifier>DOI: 10.1016/j.jbiomech.2009.06.041</identifier><identifier>PMID: 19665133</identifier><language>eng</language><publisher>United States: Elsevier Ltd</publisher><subject>Animals ; Cell Survival ; Cell viability ; Compliance ; Computer Simulation ; Disease Models, Animal ; Elastic Modulus ; Elasticity ; Experiments ; Humans ; mdx tendon ; Mechanical properties ; Mice ; Mice, Inbred mdx ; Models, Biological ; Muscular Dystrophies - pathology ; Muscular Dystrophies - physiopathology ; Muscular dystrophy ; Muscular system ; Musculoskeletal system ; Personal relationships ; Physical Medicine and Rehabilitation ; Rodents ; Stress, Mechanical ; Tendons - pathology ; Tendons - physiopathology ; Tensile Strength ; Viscoelasticity measurement ; Viscosity ; Volterra–Wiener kernels</subject><ispartof>Journal of biomechanics, 2009-10, Vol.42 (14), p.2243-2248</ispartof><rights>Elsevier Ltd</rights><rights>2009 Elsevier Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c481t-2386472f1a64d5e526e185460d69074f6cc3f7f01bd9e87307c1a87b0547eafa3</citedby><cites>FETCH-LOGICAL-c481t-2386472f1a64d5e526e185460d69074f6cc3f7f01bd9e87307c1a87b0547eafa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1034948566?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19665133$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rizzuto, E</creatorcontrib><creatorcontrib>Musarò, A</creatorcontrib><creatorcontrib>Catizone, A</creatorcontrib><creatorcontrib>Del Prete, Z</creatorcontrib><title>Measuring tendon properties in mdx mice: Cell viability and viscoelastic characteristics</title><title>Journal of biomechanics</title><addtitle>J Biomech</addtitle><description>Abstract Muscular dystrophy is a genetic disorder of skeletal muscle characterized by progressive muscle weakness. Here we assessed whether muscle wasting affects cell viability and mechanical properties of extensor digitorum longus (EDL) and of tibialis anterior (TA) tendons from mdx dystrophic mice compared to wild type (WT) mice. mdx mice represent the classical animal model for human Duchenne muscular dystrophy, and show several signs of the pathology, including a decrease in specific force and an increase of fibrotic index. Cell viability of tendons was evaluated by histological analysis, and viscoelastic properties have been assessed by a rapid measurement protocol that allowed us to compute, at the same time, tissue complex compliance for all the frequencies of interest. Confocal microscopy and mechanical properties measurements revealed that mdx tendons, compared to WT ones, have an increase in the number of dead cells and a significant reduction in tissue elasticity for all the frequencies that were tested. These findings indicate a reduced quality of the tissue. Moreover, mdx tendons have an increase in the viscous response, indicating that during dynamic loading, they dissipate more energy compared to WT. Our results demonstrate that muscular dystrophy involves not only muscle wasting, but also alteration in the viscoelastic properties of tendons, suggesting a paracrine effect of altered skeletal muscle on tendinous tissue.</description><subject>Animals</subject><subject>Cell Survival</subject><subject>Cell viability</subject><subject>Compliance</subject><subject>Computer Simulation</subject><subject>Disease Models, Animal</subject><subject>Elastic Modulus</subject><subject>Elasticity</subject><subject>Experiments</subject><subject>Humans</subject><subject>mdx tendon</subject><subject>Mechanical properties</subject><subject>Mice</subject><subject>Mice, Inbred mdx</subject><subject>Models, Biological</subject><subject>Muscular Dystrophies - pathology</subject><subject>Muscular Dystrophies - physiopathology</subject><subject>Muscular dystrophy</subject><subject>Muscular system</subject><subject>Musculoskeletal system</subject><subject>Personal relationships</subject><subject>Physical Medicine and Rehabilitation</subject><subject>Rodents</subject><subject>Stress, Mechanical</subject><subject>Tendons - pathology</subject><subject>Tendons - physiopathology</subject><subject>Tensile Strength</subject><subject>Viscoelasticity measurement</subject><subject>Viscosity</subject><subject>Volterra–Wiener kernels</subject><issn>0021-9290</issn><issn>1873-2380</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkk-LFDEQxYMo7uzqV1gCgp6mrXTSSdqDKIOrwooHFbyFdFLtpu0_Y9K9ON_eNDOysAeFQCj4VeW9vCLkkkHBgMmXXdE1YRrQ3RQlQF2ALECwB2TDtOLbkmt4SDYAJdvWZQ1n5DylDgCUUPVjcsZqKSvG-YZ8_4Q2LTGMP-iMo59Guo_THuMcMNEw0sH_pkNw-IrusO_pbbBN6MN8oHb0uUpuwt6mOTjqbmy0bsYY1jI9IY9a2yd8erovyLerd193H7bXn99_3L293jqh2bwqlUKVLbNS-AqrUiLTlZDgZZ3VttI53qoWWONrzNZAOWa1aqASCm1r-QV5cZybdf9aMM1myKqyVjvitCSjuAAFSolMPv8nyYXWutKQwWf3wG5a4phdGAZc1EJXUmZKHikXp5QitmYfw2DjIUNmzch05m9GZs3IgDQ5o9x4eRq_NAP6u7ZTKBl4cwQw_9ttwGiSCzg69CGim42fwv_feH1vhOvDGJztf-IB050fk0oD5su6KeuiQD482-N_AK_huhU</recordid><startdate>20091016</startdate><enddate>20091016</enddate><creator>Rizzuto, E</creator><creator>Musarò, A</creator><creator>Catizone, A</creator><creator>Del Prete, Z</creator><general>Elsevier Ltd</general><general>Elsevier Limited</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>3V.</scope><scope>7QP</scope><scope>7TB</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20091016</creationdate><title>Measuring tendon properties in mdx mice: Cell viability and viscoelastic characteristics</title><author>Rizzuto, E ; Musarò, A ; Catizone, A ; Del Prete, Z</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c481t-2386472f1a64d5e526e185460d69074f6cc3f7f01bd9e87307c1a87b0547eafa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Cell Survival</topic><topic>Cell viability</topic><topic>Compliance</topic><topic>Computer Simulation</topic><topic>Disease Models, Animal</topic><topic>Elastic Modulus</topic><topic>Elasticity</topic><topic>Experiments</topic><topic>Humans</topic><topic>mdx tendon</topic><topic>Mechanical properties</topic><topic>Mice</topic><topic>Mice, Inbred mdx</topic><topic>Models, Biological</topic><topic>Muscular Dystrophies - pathology</topic><topic>Muscular Dystrophies - physiopathology</topic><topic>Muscular dystrophy</topic><topic>Muscular system</topic><topic>Musculoskeletal system</topic><topic>Personal relationships</topic><topic>Physical Medicine and Rehabilitation</topic><topic>Rodents</topic><topic>Stress, Mechanical</topic><topic>Tendons - pathology</topic><topic>Tendons - physiopathology</topic><topic>Tensile Strength</topic><topic>Viscoelasticity measurement</topic><topic>Viscosity</topic><topic>Volterra–Wiener kernels</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rizzuto, E</creatorcontrib><creatorcontrib>Musarò, A</creatorcontrib><creatorcontrib>Catizone, A</creatorcontrib><creatorcontrib>Del Prete, Z</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Mechanical & Transportation Engineering Abstracts</collection><collection>Physical Education Index</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>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>Research Library (Alumni Edition)</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>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>Research Library Prep</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>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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 China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of biomechanics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rizzuto, E</au><au>Musarò, A</au><au>Catizone, A</au><au>Del Prete, Z</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Measuring tendon properties in mdx mice: Cell viability and viscoelastic characteristics</atitle><jtitle>Journal of biomechanics</jtitle><addtitle>J Biomech</addtitle><date>2009-10-16</date><risdate>2009</risdate><volume>42</volume><issue>14</issue><spage>2243</spage><epage>2248</epage><pages>2243-2248</pages><issn>0021-9290</issn><eissn>1873-2380</eissn><abstract>Abstract Muscular dystrophy is a genetic disorder of skeletal muscle characterized by progressive muscle weakness. Here we assessed whether muscle wasting affects cell viability and mechanical properties of extensor digitorum longus (EDL) and of tibialis anterior (TA) tendons from mdx dystrophic mice compared to wild type (WT) mice. mdx mice represent the classical animal model for human Duchenne muscular dystrophy, and show several signs of the pathology, including a decrease in specific force and an increase of fibrotic index. Cell viability of tendons was evaluated by histological analysis, and viscoelastic properties have been assessed by a rapid measurement protocol that allowed us to compute, at the same time, tissue complex compliance for all the frequencies of interest. Confocal microscopy and mechanical properties measurements revealed that mdx tendons, compared to WT ones, have an increase in the number of dead cells and a significant reduction in tissue elasticity for all the frequencies that were tested. These findings indicate a reduced quality of the tissue. Moreover, mdx tendons have an increase in the viscous response, indicating that during dynamic loading, they dissipate more energy compared to WT. Our results demonstrate that muscular dystrophy involves not only muscle wasting, but also alteration in the viscoelastic properties of tendons, suggesting a paracrine effect of altered skeletal muscle on tendinous tissue.</abstract><cop>United States</cop><pub>Elsevier Ltd</pub><pmid>19665133</pmid><doi>10.1016/j.jbiomech.2009.06.041</doi><tpages>6</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0021-9290 |
ispartof | Journal of biomechanics, 2009-10, Vol.42 (14), p.2243-2248 |
issn | 0021-9290 1873-2380 |
language | eng |
recordid | cdi_proquest_miscellaneous_734070774 |
source | MEDLINE; ScienceDirect Journals (5 years ago - present); ProQuest Central UK/Ireland |
subjects | Animals Cell Survival Cell viability Compliance Computer Simulation Disease Models, Animal Elastic Modulus Elasticity Experiments Humans mdx tendon Mechanical properties Mice Mice, Inbred mdx Models, Biological Muscular Dystrophies - pathology Muscular Dystrophies - physiopathology Muscular dystrophy Muscular system Musculoskeletal system Personal relationships Physical Medicine and Rehabilitation Rodents Stress, Mechanical Tendons - pathology Tendons - physiopathology Tensile Strength Viscoelasticity measurement Viscosity Volterra–Wiener kernels |
title | Measuring tendon properties in mdx mice: Cell viability and viscoelastic characteristics |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T04%3A47%3A41IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Measuring%20tendon%20properties%20in%20mdx%20mice:%20Cell%20viability%20and%20viscoelastic%20characteristics&rft.jtitle=Journal%20of%20biomechanics&rft.au=Rizzuto,%20E&rft.date=2009-10-16&rft.volume=42&rft.issue=14&rft.spage=2243&rft.epage=2248&rft.pages=2243-2248&rft.issn=0021-9290&rft.eissn=1873-2380&rft_id=info:doi/10.1016/j.jbiomech.2009.06.041&rft_dat=%3Cproquest_cross%3E2744239331%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1034948566&rft_id=info:pmid/19665133&rft_els_id=1_s2_0_S0021929009003856&rfr_iscdi=true |