An anti-inflammatory role for leukemia inhibitory factor receptor signaling in regenerating skeletal muscle
Skeletal muscle regeneration in pathology and following injury requires the coordinated actions of inflammatory cells and myogenic cells to remove damaged tissue and rebuild syncytial muscle cells, respectively. Following contusion injury to muscle, the cytokine leukemia inhibitor factor (LIF) is up...
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| Veröffentlicht in: | Histochemistry and cell biology 2013, Vol.139 (1), p.13-34 |
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| creator | Hunt, Liam C. Upadhyay, Aradhana Jazayeri, Jalal A. Tudor, Elizabeth M. White, Jason D. |
| description | Skeletal muscle regeneration in pathology and following injury requires the coordinated actions of inflammatory cells and myogenic cells to remove damaged tissue and rebuild syncytial muscle cells, respectively. Following contusion injury to muscle, the cytokine leukemia inhibitor factor (LIF) is up-regulated and knockout of
Lif
negatively impacts on morphometric parameters of muscle regeneration. Although it was speculated that LIF regulates muscle regeneration through direct effects on myogenic cells, the inflammatory effects of LIF have not been examined in regenerating skeletal muscle. Therefore, the expression and function of LIF was examined using the antagonist MH35-BD during specific inflammatory and myogenic stages of notexin-induced muscle regeneration in mice. LIF protein and mRNA were up-regulated in two distinct phases following intramuscular injection of notexin into tibialis anterior muscles. The first phase of LIF up-regulation coincided with the increased expression of pro-inflammatory cytokines; the second phase coincided with myogenic differentiation and formation of new myotubes. Administration of the LIF receptor antagonist MH35-BD during the second phase of LIF up-regulation had no significant effects on transcript expression of genes required for myogenic differentiation or associated with inflammation; there were no significant differences in morphometric parameters of the regenerating muscle. Conversely, when MH35-BD was administered during the acute inflammatory phase, increased gene transcripts for the pro-inflammatory cytokines
Tnf
(Tumor necrosis factor),
Il1b
(Interleukin-1β) and
Il6
(Interleukin-6) alongside an increase in the number of Ly6G positive neutrophils infiltrating the muscle were observed. This was followed by a reduction in
Myog
(Myogenin) mRNA, which is required for myogenic differentiation, and the subsequent number of myotubes formed was significantly decreased in MH35-BD-treated groups compared to sham. Thus, antagonism of the LIF receptor during the inflammatory phase of skeletal muscle regeneration appeared to induce an inflammatory response that inhibited subsequent myotube formation. We propose that the predominant role of LIF in skeletal muscle regeneration appears to be in regulating the inflammatory response rather than directly effecting myogenic cells. |
| doi_str_mv | 10.1007/s00418-012-1018-0 |
| format | Article |
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Lif
negatively impacts on morphometric parameters of muscle regeneration. Although it was speculated that LIF regulates muscle regeneration through direct effects on myogenic cells, the inflammatory effects of LIF have not been examined in regenerating skeletal muscle. Therefore, the expression and function of LIF was examined using the antagonist MH35-BD during specific inflammatory and myogenic stages of notexin-induced muscle regeneration in mice. LIF protein and mRNA were up-regulated in two distinct phases following intramuscular injection of notexin into tibialis anterior muscles. The first phase of LIF up-regulation coincided with the increased expression of pro-inflammatory cytokines; the second phase coincided with myogenic differentiation and formation of new myotubes. Administration of the LIF receptor antagonist MH35-BD during the second phase of LIF up-regulation had no significant effects on transcript expression of genes required for myogenic differentiation or associated with inflammation; there were no significant differences in morphometric parameters of the regenerating muscle. Conversely, when MH35-BD was administered during the acute inflammatory phase, increased gene transcripts for the pro-inflammatory cytokines
Tnf
(Tumor necrosis factor),
Il1b
(Interleukin-1β) and
Il6
(Interleukin-6) alongside an increase in the number of Ly6G positive neutrophils infiltrating the muscle were observed. This was followed by a reduction in
Myog
(Myogenin) mRNA, which is required for myogenic differentiation, and the subsequent number of myotubes formed was significantly decreased in MH35-BD-treated groups compared to sham. Thus, antagonism of the LIF receptor during the inflammatory phase of skeletal muscle regeneration appeared to induce an inflammatory response that inhibited subsequent myotube formation. We propose that the predominant role of LIF in skeletal muscle regeneration appears to be in regulating the inflammatory response rather than directly effecting myogenic cells.</description><identifier>ISSN: 0948-6143</identifier><identifier>EISSN: 1432-119X</identifier><identifier>DOI: 10.1007/s00418-012-1018-0</identifier><identifier>PMID: 22926285</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Animals ; Biochemistry ; Biomedical and Life Sciences ; Biomedical research ; Biomedicine ; Cell Biology ; Cells, Cultured ; Cellular biology ; Cytokines ; Cytokines - genetics ; Cytokines - metabolism ; Developmental Biology ; Elapid Venoms - pharmacology ; Gene Expression Regulation ; Inflammation - genetics ; Inflammation - immunology ; Inflammation - metabolism ; Inflammation - pathology ; Inflammation - prevention & control ; Inflammation Mediators - metabolism ; Injections, Intraperitoneal ; Leukemia ; Leukemia Inhibitory Factor - administration & dosage ; Leukemia Inhibitory Factor - genetics ; Leukemia Inhibitory Factor - metabolism ; Leukemia Inhibitory Factor Receptor alpha Subunit - antagonists & inhibitors ; Leukemia Inhibitory Factor Receptor alpha Subunit - metabolism ; Macrophages - immunology ; Macrophages - metabolism ; Male ; Mast Cells - immunology ; Mast Cells - metabolism ; Mice ; Mice, Inbred C57BL ; Muscle Development - drug effects ; Muscle, Skeletal - drug effects ; Muscle, Skeletal - immunology ; Muscle, Skeletal - metabolism ; Muscle, Skeletal - pathology ; Mutation ; Myogenin - genetics ; Myogenin - metabolism ; Neuromuscular diseases ; Neutrophils - immunology ; Neutrophils - metabolism ; Original Paper ; Recombinant Proteins - administration & dosage ; Regeneration - drug effects ; RNA, Messenger - metabolism ; Signal Transduction - drug effects ; Time Factors</subject><ispartof>Histochemistry and cell biology, 2013, Vol.139 (1), p.13-34</ispartof><rights>Springer-Verlag 2012</rights><rights>Springer-Verlag Berlin Heidelberg 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-d9ded4ccba1aa1df5e8f3bf5a3931cc846355d684b9e945797f6e5a21c45b4f63</citedby><cites>FETCH-LOGICAL-c415t-d9ded4ccba1aa1df5e8f3bf5a3931cc846355d684b9e945797f6e5a21c45b4f63</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/s00418-012-1018-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00418-012-1018-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22926285$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hunt, Liam C.</creatorcontrib><creatorcontrib>Upadhyay, Aradhana</creatorcontrib><creatorcontrib>Jazayeri, Jalal A.</creatorcontrib><creatorcontrib>Tudor, Elizabeth M.</creatorcontrib><creatorcontrib>White, Jason D.</creatorcontrib><title>An anti-inflammatory role for leukemia inhibitory factor receptor signaling in regenerating skeletal muscle</title><title>Histochemistry and cell biology</title><addtitle>Histochem Cell Biol</addtitle><addtitle>Histochem Cell Biol</addtitle><description>Skeletal muscle regeneration in pathology and following injury requires the coordinated actions of inflammatory cells and myogenic cells to remove damaged tissue and rebuild syncytial muscle cells, respectively. Following contusion injury to muscle, the cytokine leukemia inhibitor factor (LIF) is up-regulated and knockout of
Lif
negatively impacts on morphometric parameters of muscle regeneration. Although it was speculated that LIF regulates muscle regeneration through direct effects on myogenic cells, the inflammatory effects of LIF have not been examined in regenerating skeletal muscle. Therefore, the expression and function of LIF was examined using the antagonist MH35-BD during specific inflammatory and myogenic stages of notexin-induced muscle regeneration in mice. LIF protein and mRNA were up-regulated in two distinct phases following intramuscular injection of notexin into tibialis anterior muscles. The first phase of LIF up-regulation coincided with the increased expression of pro-inflammatory cytokines; the second phase coincided with myogenic differentiation and formation of new myotubes. Administration of the LIF receptor antagonist MH35-BD during the second phase of LIF up-regulation had no significant effects on transcript expression of genes required for myogenic differentiation or associated with inflammation; there were no significant differences in morphometric parameters of the regenerating muscle. Conversely, when MH35-BD was administered during the acute inflammatory phase, increased gene transcripts for the pro-inflammatory cytokines
Tnf
(Tumor necrosis factor),
Il1b
(Interleukin-1β) and
Il6
(Interleukin-6) alongside an increase in the number of Ly6G positive neutrophils infiltrating the muscle were observed. This was followed by a reduction in
Myog
(Myogenin) mRNA, which is required for myogenic differentiation, and the subsequent number of myotubes formed was significantly decreased in MH35-BD-treated groups compared to sham. Thus, antagonism of the LIF receptor during the inflammatory phase of skeletal muscle regeneration appeared to induce an inflammatory response that inhibited subsequent myotube formation. We propose that the predominant role of LIF in skeletal muscle regeneration appears to be in regulating the inflammatory response rather than directly effecting myogenic cells.</description><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedical research</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cells, Cultured</subject><subject>Cellular biology</subject><subject>Cytokines</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Developmental Biology</subject><subject>Elapid Venoms - pharmacology</subject><subject>Gene Expression Regulation</subject><subject>Inflammation - genetics</subject><subject>Inflammation - immunology</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Inflammation - prevention & control</subject><subject>Inflammation Mediators - metabolism</subject><subject>Injections, Intraperitoneal</subject><subject>Leukemia</subject><subject>Leukemia Inhibitory Factor - administration & dosage</subject><subject>Leukemia Inhibitory Factor - genetics</subject><subject>Leukemia Inhibitory Factor - metabolism</subject><subject>Leukemia Inhibitory Factor Receptor alpha Subunit - antagonists & inhibitors</subject><subject>Leukemia Inhibitory Factor Receptor alpha Subunit - metabolism</subject><subject>Macrophages - immunology</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Mast Cells - immunology</subject><subject>Mast Cells - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Muscle Development - drug effects</subject><subject>Muscle, Skeletal - drug effects</subject><subject>Muscle, Skeletal - immunology</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Muscle, Skeletal - pathology</subject><subject>Mutation</subject><subject>Myogenin - genetics</subject><subject>Myogenin - metabolism</subject><subject>Neuromuscular diseases</subject><subject>Neutrophils - immunology</subject><subject>Neutrophils - metabolism</subject><subject>Original Paper</subject><subject>Recombinant Proteins - administration & dosage</subject><subject>Regeneration - drug effects</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Time Factors</subject><issn>0948-6143</issn><issn>1432-119X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kU1P3DAQhq2qqLtAf0AvVaReegl4HDuJjwhRQELiAhI3y3HGW-86ztZODvx7HBaqqhKn-XrmHdkvId-AngGlzXmilENbUmAl0CX5RNbAq1yBfPpM1lTytqxzZ0WOU9pSCkIy9oWsGJOsZq1Yk91FKHSYXOmC9XoY9DTG5yKOHgs7xsLjvMPB6cKF365zr0OrTY5FRIP7JUluE7R3YZOh3N1gwKinpU479DhpXwxzMh5PyZHVPuHXt3hCHn9dPVzelHf317eXF3el4SCmspc99tyYToPW0FuBra06K3QlKzCm5XUlRF-3vJMouWhkY2sUmoHhouO2rk7Iz4PuPo5_ZkyTGlwy6L0OOM5JAWsqqKmQTUZ__Iduxznm52SK19CIBuhCwYEycUwpolX76AYdnxVQtTihDk6o7IRanFA073x_U567Afu_G-9fnwF2AFIehQ3Gf05_qPoC4oeVYw</recordid><startdate>2013</startdate><enddate>2013</enddate><creator>Hunt, Liam C.</creator><creator>Upadhyay, Aradhana</creator><creator>Jazayeri, Jalal A.</creator><creator>Tudor, Elizabeth M.</creator><creator>White, Jason D.</creator><general>Springer-Verlag</general><general>Springer Nature B.V</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>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>2013</creationdate><title>An anti-inflammatory role for leukemia inhibitory factor receptor signaling in regenerating skeletal muscle</title><author>Hunt, Liam C. ; Upadhyay, Aradhana ; Jazayeri, Jalal A. ; Tudor, Elizabeth M. ; White, Jason D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-d9ded4ccba1aa1df5e8f3bf5a3931cc846355d684b9e945797f6e5a21c45b4f63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedical research</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cells, Cultured</topic><topic>Cellular biology</topic><topic>Cytokines</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Developmental Biology</topic><topic>Elapid Venoms - pharmacology</topic><topic>Gene Expression Regulation</topic><topic>Inflammation - genetics</topic><topic>Inflammation - immunology</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Inflammation - prevention & control</topic><topic>Inflammation Mediators - metabolism</topic><topic>Injections, Intraperitoneal</topic><topic>Leukemia</topic><topic>Leukemia Inhibitory Factor - administration & dosage</topic><topic>Leukemia Inhibitory Factor - genetics</topic><topic>Leukemia Inhibitory Factor - metabolism</topic><topic>Leukemia Inhibitory Factor Receptor alpha Subunit - antagonists & inhibitors</topic><topic>Leukemia Inhibitory Factor Receptor alpha Subunit - metabolism</topic><topic>Macrophages - immunology</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Mast Cells - immunology</topic><topic>Mast Cells - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Muscle Development - drug effects</topic><topic>Muscle, Skeletal - drug effects</topic><topic>Muscle, Skeletal - immunology</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Muscle, Skeletal - pathology</topic><topic>Mutation</topic><topic>Myogenin - genetics</topic><topic>Myogenin - metabolism</topic><topic>Neuromuscular diseases</topic><topic>Neutrophils - immunology</topic><topic>Neutrophils - metabolism</topic><topic>Original Paper</topic><topic>Recombinant Proteins - administration & dosage</topic><topic>Regeneration - drug effects</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hunt, Liam C.</creatorcontrib><creatorcontrib>Upadhyay, Aradhana</creatorcontrib><creatorcontrib>Jazayeri, Jalal A.</creatorcontrib><creatorcontrib>Tudor, Elizabeth M.</creatorcontrib><creatorcontrib>White, Jason D.</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>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</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>ProQuest Pharma Collection</collection><collection>Public Health 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>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>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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>MEDLINE - Academic</collection><jtitle>Histochemistry and cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hunt, Liam C.</au><au>Upadhyay, Aradhana</au><au>Jazayeri, Jalal A.</au><au>Tudor, Elizabeth M.</au><au>White, Jason D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>An anti-inflammatory role for leukemia inhibitory factor receptor signaling in regenerating skeletal muscle</atitle><jtitle>Histochemistry and cell biology</jtitle><stitle>Histochem Cell Biol</stitle><addtitle>Histochem Cell Biol</addtitle><date>2013</date><risdate>2013</risdate><volume>139</volume><issue>1</issue><spage>13</spage><epage>34</epage><pages>13-34</pages><issn>0948-6143</issn><eissn>1432-119X</eissn><abstract>Skeletal muscle regeneration in pathology and following injury requires the coordinated actions of inflammatory cells and myogenic cells to remove damaged tissue and rebuild syncytial muscle cells, respectively. Following contusion injury to muscle, the cytokine leukemia inhibitor factor (LIF) is up-regulated and knockout of
Lif
negatively impacts on morphometric parameters of muscle regeneration. Although it was speculated that LIF regulates muscle regeneration through direct effects on myogenic cells, the inflammatory effects of LIF have not been examined in regenerating skeletal muscle. Therefore, the expression and function of LIF was examined using the antagonist MH35-BD during specific inflammatory and myogenic stages of notexin-induced muscle regeneration in mice. LIF protein and mRNA were up-regulated in two distinct phases following intramuscular injection of notexin into tibialis anterior muscles. The first phase of LIF up-regulation coincided with the increased expression of pro-inflammatory cytokines; the second phase coincided with myogenic differentiation and formation of new myotubes. Administration of the LIF receptor antagonist MH35-BD during the second phase of LIF up-regulation had no significant effects on transcript expression of genes required for myogenic differentiation or associated with inflammation; there were no significant differences in morphometric parameters of the regenerating muscle. Conversely, when MH35-BD was administered during the acute inflammatory phase, increased gene transcripts for the pro-inflammatory cytokines
Tnf
(Tumor necrosis factor),
Il1b
(Interleukin-1β) and
Il6
(Interleukin-6) alongside an increase in the number of Ly6G positive neutrophils infiltrating the muscle were observed. This was followed by a reduction in
Myog
(Myogenin) mRNA, which is required for myogenic differentiation, and the subsequent number of myotubes formed was significantly decreased in MH35-BD-treated groups compared to sham. Thus, antagonism of the LIF receptor during the inflammatory phase of skeletal muscle regeneration appeared to induce an inflammatory response that inhibited subsequent myotube formation. We propose that the predominant role of LIF in skeletal muscle regeneration appears to be in regulating the inflammatory response rather than directly effecting myogenic cells.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>22926285</pmid><doi>10.1007/s00418-012-1018-0</doi><tpages>22</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 0948-6143 1432-119X |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Animals Biochemistry Biomedical and Life Sciences Biomedical research Biomedicine Cell Biology Cells, Cultured Cellular biology Cytokines Cytokines - genetics Cytokines - metabolism Developmental Biology Elapid Venoms - pharmacology Gene Expression Regulation Inflammation - genetics Inflammation - immunology Inflammation - metabolism Inflammation - pathology Inflammation - prevention & control Inflammation Mediators - metabolism Injections, Intraperitoneal Leukemia Leukemia Inhibitory Factor - administration & dosage Leukemia Inhibitory Factor - genetics Leukemia Inhibitory Factor - metabolism Leukemia Inhibitory Factor Receptor alpha Subunit - antagonists & inhibitors Leukemia Inhibitory Factor Receptor alpha Subunit - metabolism Macrophages - immunology Macrophages - metabolism Male Mast Cells - immunology Mast Cells - metabolism Mice Mice, Inbred C57BL Muscle Development - drug effects Muscle, Skeletal - drug effects Muscle, Skeletal - immunology Muscle, Skeletal - metabolism Muscle, Skeletal - pathology Mutation Myogenin - genetics Myogenin - metabolism Neuromuscular diseases Neutrophils - immunology Neutrophils - metabolism Original Paper Recombinant Proteins - administration & dosage Regeneration - drug effects RNA, Messenger - metabolism Signal Transduction - drug effects Time Factors |
| title | An anti-inflammatory role for leukemia inhibitory factor receptor signaling in regenerating skeletal muscle |
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