A potential new role for myofibroblasts in remodeling of sub-rupture fatigue tendon injuries by exercise
Tendons are ineffective at repairing sub-rupture fatigue injuries. Accordingly, we evaluated whether an exercise protocol that we have previously found to decrease structural damage kinks in fatigue damaged tendons, leads to improvement in mechanical properties. We hypothesized that exercise that pr...
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| Veröffentlicht in: | Scientific reports 2018-06, Vol.8 (1), p.8933-10, Article 8933 |
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| creator | Bell, Rebecca Gendron, N. Remi Anderson, Matthew Flatow, Evan L. Andarawis-Puri, Nelly |
| description | Tendons are ineffective at repairing sub-rupture fatigue injuries. Accordingly, we evaluated whether an exercise protocol that we have previously found to decrease structural damage kinks in fatigue damaged tendons, leads to improvement in mechanical properties. We hypothesized that exercise that promotes repair of fatigue damage will decrease apoptosis and increase the population of myofibroblasts. Rat patellar tendons underwent
in vivo
fatigue loading for 500 or 7200 cycles. Animals resumed cage activity for 2-weeks, then either remained cage active or began treadmill running until sacrifice at 4- or 10-weeks post-fatigue loading. Exercise following fatigue damage increased the stiffness back towards naïve levels, decreased apoptosis and increased the population of myofibroblasts. Next, proteins associated with inhibition of apoptosis (Collagen VI) or activation of myofibroblast (pSmad 2/3, fibrillin, integrin subunits αV and α5) were evaluated. Data suggests that collagen VI may not be integral to inhibition of apoptosis in this context. Exercise increased pSmad 2/3 and fibrillin in the insertion region for the 7200-cycles group. In addition, exercise decreased integrin αV and increased integrin α5 in fatigue damaged tendons. Data suggests that a decrease in apoptosis and an increase in population of myofibroblasts may be integral to remodeling of fatigue damaged tendons. |
| doi_str_mv | 10.1038/s41598-018-27196-5 |
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in vivo
fatigue loading for 500 or 7200 cycles. Animals resumed cage activity for 2-weeks, then either remained cage active or began treadmill running until sacrifice at 4- or 10-weeks post-fatigue loading. Exercise following fatigue damage increased the stiffness back towards naïve levels, decreased apoptosis and increased the population of myofibroblasts. Next, proteins associated with inhibition of apoptosis (Collagen VI) or activation of myofibroblast (pSmad 2/3, fibrillin, integrin subunits αV and α5) were evaluated. Data suggests that collagen VI may not be integral to inhibition of apoptosis in this context. Exercise increased pSmad 2/3 and fibrillin in the insertion region for the 7200-cycles group. In addition, exercise decreased integrin αV and increased integrin α5 in fatigue damaged tendons. Data suggests that a decrease in apoptosis and an increase in population of myofibroblasts may be integral to remodeling of fatigue damaged tendons.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-018-27196-5</identifier><identifier>PMID: 29895865</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/51 ; 631/443 ; 631/45 ; 82 ; Apoptosis ; Collagen ; Fatigue ; Fibrillin ; Humanities and Social Sciences ; Injuries ; Mechanical properties ; multidisciplinary ; Physical training ; Rupture ; Science ; Science (multidisciplinary) ; Tendons</subject><ispartof>Scientific reports, 2018-06, Vol.8 (1), p.8933-10, Article 8933</ispartof><rights>The Author(s) 2018</rights><rights>2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c532t-10ae88ecd6a477ab42c507891972ebe6df39d9ae60af9d7eef004994183f5ae63</citedby><cites>FETCH-LOGICAL-c532t-10ae88ecd6a477ab42c507891972ebe6df39d9ae60af9d7eef004994183f5ae63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5997675/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5997675/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,41120,42189,51576,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29895865$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bell, Rebecca</creatorcontrib><creatorcontrib>Gendron, N. Remi</creatorcontrib><creatorcontrib>Anderson, Matthew</creatorcontrib><creatorcontrib>Flatow, Evan L.</creatorcontrib><creatorcontrib>Andarawis-Puri, Nelly</creatorcontrib><title>A potential new role for myofibroblasts in remodeling of sub-rupture fatigue tendon injuries by exercise</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Tendons are ineffective at repairing sub-rupture fatigue injuries. Accordingly, we evaluated whether an exercise protocol that we have previously found to decrease structural damage kinks in fatigue damaged tendons, leads to improvement in mechanical properties. We hypothesized that exercise that promotes repair of fatigue damage will decrease apoptosis and increase the population of myofibroblasts. Rat patellar tendons underwent
in vivo
fatigue loading for 500 or 7200 cycles. Animals resumed cage activity for 2-weeks, then either remained cage active or began treadmill running until sacrifice at 4- or 10-weeks post-fatigue loading. Exercise following fatigue damage increased the stiffness back towards naïve levels, decreased apoptosis and increased the population of myofibroblasts. Next, proteins associated with inhibition of apoptosis (Collagen VI) or activation of myofibroblast (pSmad 2/3, fibrillin, integrin subunits αV and α5) were evaluated. Data suggests that collagen VI may not be integral to inhibition of apoptosis in this context. Exercise increased pSmad 2/3 and fibrillin in the insertion region for the 7200-cycles group. In addition, exercise decreased integrin αV and increased integrin α5 in fatigue damaged tendons. 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Remi ; Anderson, Matthew ; Flatow, Evan L. ; Andarawis-Puri, Nelly</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c532t-10ae88ecd6a477ab42c507891972ebe6df39d9ae60af9d7eef004994183f5ae63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>13</topic><topic>13/51</topic><topic>631/443</topic><topic>631/45</topic><topic>82</topic><topic>Apoptosis</topic><topic>Collagen</topic><topic>Fatigue</topic><topic>Fibrillin</topic><topic>Humanities and Social Sciences</topic><topic>Injuries</topic><topic>Mechanical properties</topic><topic>multidisciplinary</topic><topic>Physical training</topic><topic>Rupture</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Tendons</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bell, Rebecca</creatorcontrib><creatorcontrib>Gendron, N. Remi</creatorcontrib><creatorcontrib>Anderson, Matthew</creatorcontrib><creatorcontrib>Flatow, Evan L.</creatorcontrib><creatorcontrib>Andarawis-Puri, Nelly</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</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 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>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</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>Biological Science Database</collection><collection>Access via ProQuest (Open Access)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bell, Rebecca</au><au>Gendron, N. Remi</au><au>Anderson, Matthew</au><au>Flatow, Evan L.</au><au>Andarawis-Puri, Nelly</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A potential new role for myofibroblasts in remodeling of sub-rupture fatigue tendon injuries by exercise</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2018-06-12</date><risdate>2018</risdate><volume>8</volume><issue>1</issue><spage>8933</spage><epage>10</epage><pages>8933-10</pages><artnum>8933</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Tendons are ineffective at repairing sub-rupture fatigue injuries. Accordingly, we evaluated whether an exercise protocol that we have previously found to decrease structural damage kinks in fatigue damaged tendons, leads to improvement in mechanical properties. We hypothesized that exercise that promotes repair of fatigue damage will decrease apoptosis and increase the population of myofibroblasts. Rat patellar tendons underwent
in vivo
fatigue loading for 500 or 7200 cycles. Animals resumed cage activity for 2-weeks, then either remained cage active or began treadmill running until sacrifice at 4- or 10-weeks post-fatigue loading. Exercise following fatigue damage increased the stiffness back towards naïve levels, decreased apoptosis and increased the population of myofibroblasts. Next, proteins associated with inhibition of apoptosis (Collagen VI) or activation of myofibroblast (pSmad 2/3, fibrillin, integrin subunits αV and α5) were evaluated. Data suggests that collagen VI may not be integral to inhibition of apoptosis in this context. Exercise increased pSmad 2/3 and fibrillin in the insertion region for the 7200-cycles group. In addition, exercise decreased integrin αV and increased integrin α5 in fatigue damaged tendons. Data suggests that a decrease in apoptosis and an increase in population of myofibroblasts may be integral to remodeling of fatigue damaged tendons.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29895865</pmid><doi>10.1038/s41598-018-27196-5</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13 13/51 631/443 631/45 82 Apoptosis Collagen Fatigue Fibrillin Humanities and Social Sciences Injuries Mechanical properties multidisciplinary Physical training Rupture Science Science (multidisciplinary) Tendons |
| title | A potential new role for myofibroblasts in remodeling of sub-rupture fatigue tendon injuries by exercise |
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