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Absence of CCR2 results in an inflammaging environment in young mice with age‐independent impairments in muscle regeneration
CCR2 KO has impaired myeloid recruitment, regeneration, and failure of regenerated myofibers to attain baseline size despite increased tissue cytokines/chemokines. Skeletal muscle regeneration requires coordination between dynamic cellular populations and tissue microenvironments. Macrophages, recru...
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| Published in: | Journal of leukocyte biology 2016-11, Vol.100 (5), p.1011-1025 |
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| creator | Melton, David W. Roberts, Alexander C. Wang, Hanzhou Sarwar, Zaheer Wetzel, Michael D. Wells, Jason T. Porter, Laurel Berton, Michael T. McManus, Linda M. Shireman, Paula K. |
| description | CCR2 KO has impaired myeloid recruitment, regeneration, and failure of regenerated myofibers to attain baseline size despite increased tissue cytokines/chemokines.
Skeletal muscle regeneration requires coordination between dynamic cellular populations and tissue microenvironments. Macrophages, recruited via CCR2, are essential for regeneration; however, the contribution of macrophages and the role of CCR2 on nonhematopoietic cells has not been defined. In addition, aging and sex interactions in regeneration and sarcopenia are unclear. Muscle regeneration was measured in young (3–6 mo), middle (11–15 mo), old (24–32 mo) male and female CCR2−/− mice. Whereas age‐related muscle atrophy/sarcopenia was present, regenerated myofiber cross‐sectional area (CSA) in CCR2−/− mice was comparably impaired across all ages and sexes, with increased adipocyte area compared with wild‐type (WT) mice. CCR2−/− mice myofibers achieved approximately one third of baseline CSA even 84 d after injury. Regenerated CSA and clearance of necrotic tissue were dependent on bone marrow–derived cellular expression of CCR2. Myogenic progenitor cells isolated from WT and CCR2−/− mice exhibited comparable proliferation and differentiation capacity. The most striking cellular anomaly in injured muscle of CCR2−/− mice was markedly decreased macrophages, with a predominance of Ly6C− anti‐inflammatory monocytes/macrophages. Ablation of proinflammatory TLR signaling did not affect muscle regeneration or resolution of necrosis. Of interest, many proinflammatory, proangiogenic, and chemotactic cytokines were markedly elevated in injured muscle of CCR2−/− relative to WT mice despite impairments in macrophage recruitment. Collectively, these results suggest that CCR2 on bone marrow–derived cells, likely macrophages, were essential to muscle regeneration independent of TLR signaling, aging, and sex. Decreased proinflammatory monocytes/macrophages actually promoted a proinflammatory microenvironment, which suggests that inflammaging was present in young CCR2−/− mice. |
| doi_str_mv | 10.1189/jlb.3MA0316-104R |
| format | article |
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Skeletal muscle regeneration requires coordination between dynamic cellular populations and tissue microenvironments. Macrophages, recruited via CCR2, are essential for regeneration; however, the contribution of macrophages and the role of CCR2 on nonhematopoietic cells has not been defined. In addition, aging and sex interactions in regeneration and sarcopenia are unclear. Muscle regeneration was measured in young (3–6 mo), middle (11–15 mo), old (24–32 mo) male and female CCR2−/− mice. Whereas age‐related muscle atrophy/sarcopenia was present, regenerated myofiber cross‐sectional area (CSA) in CCR2−/− mice was comparably impaired across all ages and sexes, with increased adipocyte area compared with wild‐type (WT) mice. CCR2−/− mice myofibers achieved approximately one third of baseline CSA even 84 d after injury. Regenerated CSA and clearance of necrotic tissue were dependent on bone marrow–derived cellular expression of CCR2. Myogenic progenitor cells isolated from WT and CCR2−/− mice exhibited comparable proliferation and differentiation capacity. The most striking cellular anomaly in injured muscle of CCR2−/− mice was markedly decreased macrophages, with a predominance of Ly6C− anti‐inflammatory monocytes/macrophages. Ablation of proinflammatory TLR signaling did not affect muscle regeneration or resolution of necrosis. Of interest, many proinflammatory, proangiogenic, and chemotactic cytokines were markedly elevated in injured muscle of CCR2−/− relative to WT mice despite impairments in macrophage recruitment. Collectively, these results suggest that CCR2 on bone marrow–derived cells, likely macrophages, were essential to muscle regeneration independent of TLR signaling, aging, and sex. Decreased proinflammatory monocytes/macrophages actually promoted a proinflammatory microenvironment, which suggests that inflammaging was present in young CCR2−/− mice.</description><identifier>ISSN: 0741-5400</identifier><identifier>EISSN: 1938-3673</identifier><identifier>DOI: 10.1189/jlb.3MA0316-104R</identifier><identifier>PMID: 27531927</identifier><language>eng</language><publisher>United States: Society for Leukocyte Biology</publisher><subject>Adaptor Proteins, Vesicular Transport - deficiency ; Aging - immunology ; Animals ; Body Weight ; Cell Cycle ; Cell Division ; Cytokines - blood ; Female ; Inflammation ; Macrophages - physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Monocytes - immunology ; Monocytes - physiology ; monocytes/macrophages ; Muscle Development ; Muscle, Skeletal - injuries ; Muscle, Skeletal - physiology ; Myeloid Differentiation Factor 88 - deficiency ; Myoblasts - pathology ; myogenic progenitor cells ; Myositis - physiopathology ; Necrosis ; Primary Research ; Radiation Chimera ; Receptors, CCR2 - deficiency ; Receptors, CCR2 - physiology ; Regeneration - physiology ; sarcopenia ; Sarcopenia - physiopathology ; Specific Pathogen-Free Organisms ; TLRs</subject><ispartof>Journal of leukocyte biology, 2016-11, Vol.100 (5), p.1011-1025</ispartof><rights>2016 Society for Leukocyte Biology</rights><rights>Society for Leukocyte Biology.</rights><rights>Society for Leukocyte Biology 2016 Society for Leukocyte Biology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5591-7d2429f93ed424ab61e15010d83e36ab8ef98dc480dfe5f5598b6cd940f5bf83</citedby><cites>FETCH-LOGICAL-c5591-7d2429f93ed424ab61e15010d83e36ab8ef98dc480dfe5f5598b6cd940f5bf83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1189%2Fjlb.3MA0316-104R$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1189%2Fjlb.3MA0316-104R$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,315,786,790,891,27957,27958,50923,51032</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27531927$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Melton, David W.</creatorcontrib><creatorcontrib>Roberts, Alexander C.</creatorcontrib><creatorcontrib>Wang, Hanzhou</creatorcontrib><creatorcontrib>Sarwar, Zaheer</creatorcontrib><creatorcontrib>Wetzel, Michael D.</creatorcontrib><creatorcontrib>Wells, Jason T.</creatorcontrib><creatorcontrib>Porter, Laurel</creatorcontrib><creatorcontrib>Berton, Michael T.</creatorcontrib><creatorcontrib>McManus, Linda M.</creatorcontrib><creatorcontrib>Shireman, Paula K.</creatorcontrib><title>Absence of CCR2 results in an inflammaging environment in young mice with age‐independent impairments in muscle regeneration</title><title>Journal of leukocyte biology</title><addtitle>J Leukoc Biol</addtitle><description>CCR2 KO has impaired myeloid recruitment, regeneration, and failure of regenerated myofibers to attain baseline size despite increased tissue cytokines/chemokines.
Skeletal muscle regeneration requires coordination between dynamic cellular populations and tissue microenvironments. Macrophages, recruited via CCR2, are essential for regeneration; however, the contribution of macrophages and the role of CCR2 on nonhematopoietic cells has not been defined. In addition, aging and sex interactions in regeneration and sarcopenia are unclear. Muscle regeneration was measured in young (3–6 mo), middle (11–15 mo), old (24–32 mo) male and female CCR2−/− mice. Whereas age‐related muscle atrophy/sarcopenia was present, regenerated myofiber cross‐sectional area (CSA) in CCR2−/− mice was comparably impaired across all ages and sexes, with increased adipocyte area compared with wild‐type (WT) mice. CCR2−/− mice myofibers achieved approximately one third of baseline CSA even 84 d after injury. Regenerated CSA and clearance of necrotic tissue were dependent on bone marrow–derived cellular expression of CCR2. Myogenic progenitor cells isolated from WT and CCR2−/− mice exhibited comparable proliferation and differentiation capacity. The most striking cellular anomaly in injured muscle of CCR2−/− mice was markedly decreased macrophages, with a predominance of Ly6C− anti‐inflammatory monocytes/macrophages. Ablation of proinflammatory TLR signaling did not affect muscle regeneration or resolution of necrosis. Of interest, many proinflammatory, proangiogenic, and chemotactic cytokines were markedly elevated in injured muscle of CCR2−/− relative to WT mice despite impairments in macrophage recruitment. Collectively, these results suggest that CCR2 on bone marrow–derived cells, likely macrophages, were essential to muscle regeneration independent of TLR signaling, aging, and sex. Decreased proinflammatory monocytes/macrophages actually promoted a proinflammatory microenvironment, which suggests that inflammaging was present in young CCR2−/− mice.</description><subject>Adaptor Proteins, Vesicular Transport - deficiency</subject><subject>Aging - immunology</subject><subject>Animals</subject><subject>Body Weight</subject><subject>Cell Cycle</subject><subject>Cell Division</subject><subject>Cytokines - blood</subject><subject>Female</subject><subject>Inflammation</subject><subject>Macrophages - physiology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Monocytes - immunology</subject><subject>Monocytes - physiology</subject><subject>monocytes/macrophages</subject><subject>Muscle Development</subject><subject>Muscle, Skeletal - injuries</subject><subject>Muscle, Skeletal - physiology</subject><subject>Myeloid Differentiation Factor 88 - deficiency</subject><subject>Myoblasts - pathology</subject><subject>myogenic progenitor cells</subject><subject>Myositis - physiopathology</subject><subject>Necrosis</subject><subject>Primary Research</subject><subject>Radiation Chimera</subject><subject>Receptors, CCR2 - deficiency</subject><subject>Receptors, CCR2 - physiology</subject><subject>Regeneration - physiology</subject><subject>sarcopenia</subject><subject>Sarcopenia - physiopathology</subject><subject>Specific Pathogen-Free Organisms</subject><subject>TLRs</subject><issn>0741-5400</issn><issn>1938-3673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNqFkc9u1DAQxi1ERZfCnRPKkUvKOLYT-4K0rPhXbYVU9W45yTh1lTiLnbTaC-IReEaeBIfdVnDiMiPN_L5vRvoIeUXhnFKp3t729Tm7XAOjZU6BXz0hK6qYzFlZsadkBRWnueAAp-R5jLcAwIoSnpHTohKMqqJake_rOqJvMBttttlcFVnAOPdTzJzPjE_V9mYYTOd8l6G_c2H0A_ppWe_HOQ0Hl8T3brrJTIe_fvx0vsUdprJAw864sPB__IY5Nj2mCx16DGZyo39BTqzpI7489jNy_fHD9eZzvv366ctmvc0bIRTNq7bghbKKYcsLbuqSIhVAoZUMWWlqiVbJtuESWovCJo2sy6ZVHKyorWRn5N3BdjfXA7ZN-iiYXu-CG0zY69E4_e_GuxvdjXdaQKlA8mTw5mgQxm8zxkkPLjbY98bjOEdNJeNKSVGyhMIBbcIYY0D7eIaCXlLTKTV9TE0vqSXJ67_fexQ8xJQAcQDuXY_7_xrqi-17CpSy34puqKM</recordid><startdate>201611</startdate><enddate>201611</enddate><creator>Melton, David W.</creator><creator>Roberts, Alexander C.</creator><creator>Wang, Hanzhou</creator><creator>Sarwar, Zaheer</creator><creator>Wetzel, Michael D.</creator><creator>Wells, Jason T.</creator><creator>Porter, Laurel</creator><creator>Berton, Michael T.</creator><creator>McManus, Linda M.</creator><creator>Shireman, Paula K.</creator><general>Society for Leukocyte Biology</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>201611</creationdate><title>Absence of CCR2 results in an inflammaging environment in young mice with age‐independent impairments in muscle regeneration</title><author>Melton, David W. ; Roberts, Alexander C. ; Wang, Hanzhou ; Sarwar, Zaheer ; Wetzel, Michael D. ; Wells, Jason T. ; Porter, Laurel ; Berton, Michael T. ; McManus, Linda M. ; Shireman, Paula K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5591-7d2429f93ed424ab61e15010d83e36ab8ef98dc480dfe5f5598b6cd940f5bf83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adaptor Proteins, Vesicular Transport - deficiency</topic><topic>Aging - immunology</topic><topic>Animals</topic><topic>Body Weight</topic><topic>Cell Cycle</topic><topic>Cell Division</topic><topic>Cytokines - blood</topic><topic>Female</topic><topic>Inflammation</topic><topic>Macrophages - physiology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Monocytes - immunology</topic><topic>Monocytes - physiology</topic><topic>monocytes/macrophages</topic><topic>Muscle Development</topic><topic>Muscle, Skeletal - injuries</topic><topic>Muscle, Skeletal - physiology</topic><topic>Myeloid Differentiation Factor 88 - deficiency</topic><topic>Myoblasts - pathology</topic><topic>myogenic progenitor cells</topic><topic>Myositis - physiopathology</topic><topic>Necrosis</topic><topic>Primary Research</topic><topic>Radiation Chimera</topic><topic>Receptors, CCR2 - deficiency</topic><topic>Receptors, CCR2 - physiology</topic><topic>Regeneration - physiology</topic><topic>sarcopenia</topic><topic>Sarcopenia - physiopathology</topic><topic>Specific Pathogen-Free Organisms</topic><topic>TLRs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Melton, David W.</creatorcontrib><creatorcontrib>Roberts, Alexander C.</creatorcontrib><creatorcontrib>Wang, Hanzhou</creatorcontrib><creatorcontrib>Sarwar, Zaheer</creatorcontrib><creatorcontrib>Wetzel, Michael D.</creatorcontrib><creatorcontrib>Wells, Jason T.</creatorcontrib><creatorcontrib>Porter, Laurel</creatorcontrib><creatorcontrib>Berton, Michael T.</creatorcontrib><creatorcontrib>McManus, Linda M.</creatorcontrib><creatorcontrib>Shireman, Paula K.</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>Journal of leukocyte biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Melton, David W.</au><au>Roberts, Alexander C.</au><au>Wang, Hanzhou</au><au>Sarwar, Zaheer</au><au>Wetzel, Michael D.</au><au>Wells, Jason T.</au><au>Porter, Laurel</au><au>Berton, Michael T.</au><au>McManus, Linda M.</au><au>Shireman, Paula K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Absence of CCR2 results in an inflammaging environment in young mice with age‐independent impairments in muscle regeneration</atitle><jtitle>Journal of leukocyte biology</jtitle><addtitle>J Leukoc Biol</addtitle><date>2016-11</date><risdate>2016</risdate><volume>100</volume><issue>5</issue><spage>1011</spage><epage>1025</epage><pages>1011-1025</pages><issn>0741-5400</issn><eissn>1938-3673</eissn><notes>Current affiliation: Shriners Hospital for Children, Houston, Texas, USA.</notes><notes>Current affiliation: Lahey Hospital & Medical Center, Burlington, Massachusetts, USA.</notes><notes>Current affiliation: Bexar County Medical Examiner's Office, San Antonio, Texas, USA.</notes><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><notes>Current affiliation: Bexar County Medical Examiner’s Office, San Antonio, Texas, USA.</notes><abstract>CCR2 KO has impaired myeloid recruitment, regeneration, and failure of regenerated myofibers to attain baseline size despite increased tissue cytokines/chemokines.
Skeletal muscle regeneration requires coordination between dynamic cellular populations and tissue microenvironments. Macrophages, recruited via CCR2, are essential for regeneration; however, the contribution of macrophages and the role of CCR2 on nonhematopoietic cells has not been defined. In addition, aging and sex interactions in regeneration and sarcopenia are unclear. Muscle regeneration was measured in young (3–6 mo), middle (11–15 mo), old (24–32 mo) male and female CCR2−/− mice. Whereas age‐related muscle atrophy/sarcopenia was present, regenerated myofiber cross‐sectional area (CSA) in CCR2−/− mice was comparably impaired across all ages and sexes, with increased adipocyte area compared with wild‐type (WT) mice. CCR2−/− mice myofibers achieved approximately one third of baseline CSA even 84 d after injury. Regenerated CSA and clearance of necrotic tissue were dependent on bone marrow–derived cellular expression of CCR2. Myogenic progenitor cells isolated from WT and CCR2−/− mice exhibited comparable proliferation and differentiation capacity. The most striking cellular anomaly in injured muscle of CCR2−/− mice was markedly decreased macrophages, with a predominance of Ly6C− anti‐inflammatory monocytes/macrophages. Ablation of proinflammatory TLR signaling did not affect muscle regeneration or resolution of necrosis. Of interest, many proinflammatory, proangiogenic, and chemotactic cytokines were markedly elevated in injured muscle of CCR2−/− relative to WT mice despite impairments in macrophage recruitment. Collectively, these results suggest that CCR2 on bone marrow–derived cells, likely macrophages, were essential to muscle regeneration independent of TLR signaling, aging, and sex. Decreased proinflammatory monocytes/macrophages actually promoted a proinflammatory microenvironment, which suggests that inflammaging was present in young CCR2−/− mice.</abstract><cop>United States</cop><pub>Society for Leukocyte Biology</pub><pmid>27531927</pmid><doi>10.1189/jlb.3MA0316-104R</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 0741-5400 1938-3673 |
| language | eng |
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| source | Wiley-Blackwell Journals; Oxford Journals Online |
| subjects | Adaptor Proteins, Vesicular Transport - deficiency Aging - immunology Animals Body Weight Cell Cycle Cell Division Cytokines - blood Female Inflammation Macrophages - physiology Male Mice Mice, Inbred C57BL Mice, Knockout Monocytes - immunology Monocytes - physiology monocytes/macrophages Muscle Development Muscle, Skeletal - injuries Muscle, Skeletal - physiology Myeloid Differentiation Factor 88 - deficiency Myoblasts - pathology myogenic progenitor cells Myositis - physiopathology Necrosis Primary Research Radiation Chimera Receptors, CCR2 - deficiency Receptors, CCR2 - physiology Regeneration - physiology sarcopenia Sarcopenia - physiopathology Specific Pathogen-Free Organisms TLRs |
| title | Absence of CCR2 results in an inflammaging environment in young mice with age‐independent impairments in muscle regeneration |
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