P.1.9 Repeated cardiotoxin treatment progresses muscle phenotype in Collagen VI deficient mice
Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder...
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| Autor*in: |
Noguchi, S. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2013transfer abstract |
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| Übergeordnetes Werk: |
Enthalten in: Sperm competition in golden cuttlefish - Guo, Haoyu ELSEVIER, 2020, official journal of the World Muscle Society, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:23 ; year:2013 ; number:9 ; pages:744 |
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| DOI / URN: |
10.1016/j.nmd.2013.06.393 |
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| 520 | |a Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies. | ||
| 520 | |a Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies. | ||
| 700 | 1 | |a Ogawa, M. |4 oth | |
| 700 | 1 | |a Nishino, I. |4 oth | |
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10.1016/j.nmd.2013.06.393 doi GBVA2013016000016.pica (DE-627)ELV022102426 (ELSEVIER)S0960-8966(13)00567-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 570 550 VZ BIODIV DE-30 fid 48.68 bkl Noguchi, S. verfasserin aut P.1.9 Repeated cardiotoxin treatment progresses muscle phenotype in Collagen VI deficient mice 2013transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies. Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies. Ogawa, M. oth Nishino, I. oth Enthalten in Elsevier Science Guo, Haoyu ELSEVIER Sperm competition in golden cuttlefish 2020 official journal of the World Muscle Society Amsterdam [u.a.] (DE-627)ELV004843940 volume:23 year:2013 number:9 pages:744 https://doi.org/10.1016/j.nmd.2013.06.393 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 48.68 Aquakultur VZ AR 23 2013 9 744 045F 610 |
| spelling |
10.1016/j.nmd.2013.06.393 doi GBVA2013016000016.pica (DE-627)ELV022102426 (ELSEVIER)S0960-8966(13)00567-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 570 550 VZ BIODIV DE-30 fid 48.68 bkl Noguchi, S. verfasserin aut P.1.9 Repeated cardiotoxin treatment progresses muscle phenotype in Collagen VI deficient mice 2013transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies. Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies. Ogawa, M. oth Nishino, I. oth Enthalten in Elsevier Science Guo, Haoyu ELSEVIER Sperm competition in golden cuttlefish 2020 official journal of the World Muscle Society Amsterdam [u.a.] (DE-627)ELV004843940 volume:23 year:2013 number:9 pages:744 https://doi.org/10.1016/j.nmd.2013.06.393 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 48.68 Aquakultur VZ AR 23 2013 9 744 045F 610 |
| allfields_unstemmed |
10.1016/j.nmd.2013.06.393 doi GBVA2013016000016.pica (DE-627)ELV022102426 (ELSEVIER)S0960-8966(13)00567-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 570 550 VZ BIODIV DE-30 fid 48.68 bkl Noguchi, S. verfasserin aut P.1.9 Repeated cardiotoxin treatment progresses muscle phenotype in Collagen VI deficient mice 2013transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies. Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies. Ogawa, M. oth Nishino, I. oth Enthalten in Elsevier Science Guo, Haoyu ELSEVIER Sperm competition in golden cuttlefish 2020 official journal of the World Muscle Society Amsterdam [u.a.] (DE-627)ELV004843940 volume:23 year:2013 number:9 pages:744 https://doi.org/10.1016/j.nmd.2013.06.393 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 48.68 Aquakultur VZ AR 23 2013 9 744 045F 610 |
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10.1016/j.nmd.2013.06.393 doi GBVA2013016000016.pica (DE-627)ELV022102426 (ELSEVIER)S0960-8966(13)00567-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 570 550 VZ BIODIV DE-30 fid 48.68 bkl Noguchi, S. verfasserin aut P.1.9 Repeated cardiotoxin treatment progresses muscle phenotype in Collagen VI deficient mice 2013transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies. Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies. Ogawa, M. oth Nishino, I. oth Enthalten in Elsevier Science Guo, Haoyu ELSEVIER Sperm competition in golden cuttlefish 2020 official journal of the World Muscle Society Amsterdam [u.a.] (DE-627)ELV004843940 volume:23 year:2013 number:9 pages:744 https://doi.org/10.1016/j.nmd.2013.06.393 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 48.68 Aquakultur VZ AR 23 2013 9 744 045F 610 |
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10.1016/j.nmd.2013.06.393 doi GBVA2013016000016.pica (DE-627)ELV022102426 (ELSEVIER)S0960-8966(13)00567-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 570 550 VZ BIODIV DE-30 fid 48.68 bkl Noguchi, S. verfasserin aut P.1.9 Repeated cardiotoxin treatment progresses muscle phenotype in Collagen VI deficient mice 2013transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies. Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies. Ogawa, M. oth Nishino, I. oth Enthalten in Elsevier Science Guo, Haoyu ELSEVIER Sperm competition in golden cuttlefish 2020 official journal of the World Muscle Society Amsterdam [u.a.] (DE-627)ELV004843940 volume:23 year:2013 number:9 pages:744 https://doi.org/10.1016/j.nmd.2013.06.393 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 48.68 Aquakultur VZ AR 23 2013 9 744 045F 610 |
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These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. 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P.1.9 Repeated cardiotoxin treatment progresses muscle phenotype in Collagen VI deficient mice |
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Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies. |
| abstractGer |
Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies. |
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Collagen VI-related myopathies are inherited muscle disorders characterized clinically by muscle weakness and pathologically by fiber size variation and enhanced fibrosis. These disorders show broad spectrum of clinical presentation from severe Ullrich congenital muscular dystrophy (UCMD) to milder Bethlem myopathy (BM), both of which and both are caused by mutations in one of Col6A1–3 genes, In mice, collagen VI deficiency has been reported to reveal remarkable phenotypes in some organs such as bones, cartilages and adipose tissues, however their skeletal muscle presents a milder phenotype as that in BM. We have generated collagen VI-deficient mice and observed their muscle pathology chronologically. Along aging, distal muscles showed fiber size variation remarkably but only milder moderate fibrosis. Since collagen VI is produced in interstitial mesenchymal cells, we hypothesized if activation of mesenchymal cells contributes the muscle pathological phenotypes in collagen VI-deficient mice. We injected cardiotoxin (CTX) to TA muscles of collagen VI-deficient mice repeatedly to induce muscle necrosis and regeneration-mediated activation of mesenchymal cells artificially. After CTX injections, myofibers were well regenerated even with multiple CTX treatment, and along the number of CTX injections, muscle weakness, myofiber atrophy and interstitial fibrosis were progressed as observed in UCMD. The finding suggests that dysregulation of interstitial mesenchymal cells may be associated with the pathogenesis of collagen VI-related myopathies. |
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