C2 and C2C12 murine skeletal myoblast models of atrophic and hypertrophic potential: relevance to disease and ageing?

2.50
Hdl Handle:
http://hdl.handle.net/10547/225832
Title:
C2 and C2C12 murine skeletal myoblast models of atrophic and hypertrophic potential: relevance to disease and ageing?
Authors:
Sharples, Adam P. ( 0000-0003-1526-9400 ) ; Al-Shanti, Nasser; Stewart, Claire E.
Abstract:
Reduced muscle mass and increased susceptibility to TNF-induced degradation accompany inflamed ageing and chronic diseases. Furthermore, C(2) myoblasts display diminished differentiation and increased susceptibility to TNF-alpha-induced cell death versus subcloned C(2)C(12) cells, providing relevant models to assess: differentiation (creatine kinase), growth (protein), death (trypan-blue) and anabolic/catabolic parameters (RT-PCR) over 72 h +/- TNF-alpha (20 ng ml(-1)). At 48 and 72 h, respectively, larger myotubes and significantly higher CK activity (320.26 +/- 6.82 vs. 30.71 +/- 2.5, P < 0.05; 544.94 +/- 27.7 vs. 39.4 +/- 3.37 mU mg ml(-1), P < 0.05), fold increases in myoD (21.45 +/- 3.12 vs. 3.97 +/- 1.76, P < 0.05; 31.07 +/- 3.1 vs. 6.82 +/- 1.93, P < 0.05) and myogenin mRNA (241.8 +/- 40 vs. 36.80 +/- 19.3, P < 0.05; 440 +/- 100.5 vs. 201.1 +/- 86, P < 0.05) were detected in C(2)C(12) versus C(2). C(2)C(12) showed significant increases in IGF-I mRNA (243.05 +/- 3.87 vs. 105.75 +/- 21.95, P < 0.05), reduced proliferation and significantly lower protein expression (1.21 +/- 0.28 vs. 1.79 +/- 0.29 mg ml(-1), P < 0.05) at 72 h versus C(2) cells. Significant temporal reductions in C(2)C(12) IGFBP2 mRNA (28.02 +/- 15.44, 13.82 +/- 8.07, 6.92 +/- 4.37, P < 0.05) contrasted increases in C(2)s (4.31 +/- 3.31, 13.02 +/- 9.92, 82.9 +/- 58.9, P < 0.05) at 0, 48 and 72 h, respectively. TNF-alpha increased cell death in C(2)s (2.67 +/- 1.54%, 34.42 +/- 5.39%, 29.71 +/- 5.79% (0, 48, 72 h), P < 0.05), yet was without effect in C(2)C(12)s at 48 h but caused a small significant increase at 72 h (9.88 +/- 4.02% (TNF-alpha) vs. 6.17 +/- 0.749% (DM), 72 h). TNF-alpha and TNFRI mRNA were unchanged; however, larger reductions in IGF-I (8.2- and 7.5-fold vs. 4.5- and 4.1-fold (48, 72 h)), IGF-IR (2-fold vs. no-significant reduction (72 h)) and IGFBP5 (3.24 vs. 1.38 (48 h) and 2.21 vs. 1.71 (72 h), P < 0.05) mRNA were observed in C(2) versus C(2)C(12) with TNF-alpha. This investigation provides insight into regulators of altered basal hypertrophy and TNF-induced atrophy, providing a model for future investigation into therapeutic initiatives for ageing/wasting disorders.
Affiliation:
Manchester Metropolitan University
Citation:
Sharples, A.P., Al-Shanti, N., and Stewart, C.E. (2010), 'C2 and C2C12 murine skeletal myoblast models of atrophic and hypertrophic potential: relevance to disease and ageing?', Journal of Cellular Physiology, 225(1) pp.240-50.
Journal:
Journal of Cellular Physiology
Issue Date:
Oct-2010
URI:
http://hdl.handle.net/10547/225832
DOI:
10.1002/jcp.22252
PubMed ID:
20506232
Type:
Article
Language:
en
ISSN:
1097-4652
Appears in Collections:
Muscle Cellular and Molecular Physiology

Full metadata record

DC FieldValue Language
dc.contributor.authorSharples, Adam P.en_GB
dc.contributor.authorAl-Shanti, Nasseren_GB
dc.contributor.authorStewart, Claire E.en_GB
dc.date.accessioned2012-05-24T15:58:58Z-
dc.date.available2012-05-24T15:58:58Z-
dc.date.issued2010-10-
dc.identifier.citationSharples, A.P., Al-Shanti, N., and Stewart, C.E. (2010), 'C2 and C2C12 murine skeletal myoblast models of atrophic and hypertrophic potential: relevance to disease and ageing?', Journal of Cellular Physiology, 225(1) pp.240-50.en_GB
dc.identifier.issn1097-4652-
dc.identifier.pmid20506232-
dc.identifier.doi10.1002/jcp.22252-
dc.identifier.urihttp://hdl.handle.net/10547/225832-
dc.description.abstractReduced muscle mass and increased susceptibility to TNF-induced degradation accompany inflamed ageing and chronic diseases. Furthermore, C(2) myoblasts display diminished differentiation and increased susceptibility to TNF-alpha-induced cell death versus subcloned C(2)C(12) cells, providing relevant models to assess: differentiation (creatine kinase), growth (protein), death (trypan-blue) and anabolic/catabolic parameters (RT-PCR) over 72 h +/- TNF-alpha (20 ng ml(-1)). At 48 and 72 h, respectively, larger myotubes and significantly higher CK activity (320.26 +/- 6.82 vs. 30.71 +/- 2.5, P < 0.05; 544.94 +/- 27.7 vs. 39.4 +/- 3.37 mU mg ml(-1), P < 0.05), fold increases in myoD (21.45 +/- 3.12 vs. 3.97 +/- 1.76, P < 0.05; 31.07 +/- 3.1 vs. 6.82 +/- 1.93, P < 0.05) and myogenin mRNA (241.8 +/- 40 vs. 36.80 +/- 19.3, P < 0.05; 440 +/- 100.5 vs. 201.1 +/- 86, P < 0.05) were detected in C(2)C(12) versus C(2). C(2)C(12) showed significant increases in IGF-I mRNA (243.05 +/- 3.87 vs. 105.75 +/- 21.95, P < 0.05), reduced proliferation and significantly lower protein expression (1.21 +/- 0.28 vs. 1.79 +/- 0.29 mg ml(-1), P < 0.05) at 72 h versus C(2) cells. Significant temporal reductions in C(2)C(12) IGFBP2 mRNA (28.02 +/- 15.44, 13.82 +/- 8.07, 6.92 +/- 4.37, P < 0.05) contrasted increases in C(2)s (4.31 +/- 3.31, 13.02 +/- 9.92, 82.9 +/- 58.9, P < 0.05) at 0, 48 and 72 h, respectively. TNF-alpha increased cell death in C(2)s (2.67 +/- 1.54%, 34.42 +/- 5.39%, 29.71 +/- 5.79% (0, 48, 72 h), P < 0.05), yet was without effect in C(2)C(12)s at 48 h but caused a small significant increase at 72 h (9.88 +/- 4.02% (TNF-alpha) vs. 6.17 +/- 0.749% (DM), 72 h). TNF-alpha and TNFRI mRNA were unchanged; however, larger reductions in IGF-I (8.2- and 7.5-fold vs. 4.5- and 4.1-fold (48, 72 h)), IGF-IR (2-fold vs. no-significant reduction (72 h)) and IGFBP5 (3.24 vs. 1.38 (48 h) and 2.21 vs. 1.71 (72 h), P < 0.05) mRNA were observed in C(2) versus C(2)C(12) with TNF-alpha. This investigation provides insight into regulators of altered basal hypertrophy and TNF-induced atrophy, providing a model for future investigation into therapeutic initiatives for ageing/wasting disorders.en_GB
dc.language.isoenen
dc.rightsArchived with thanks to Journal of cellular physiologyen_GB
dc.subject.meshAging-
dc.subject.meshAnimals-
dc.subject.meshAtrophy-
dc.subject.meshCell Death-
dc.subject.meshCell Differentiation-
dc.subject.meshCell Line-
dc.subject.meshCreatine Kinase-
dc.subject.meshHypertrophy-
dc.subject.meshInsulin-Like Growth Factor Binding Protein 2-
dc.subject.meshInsulin-Like Growth Factor Binding Protein 5-
dc.subject.meshInsulin-Like Growth Factor I-
dc.subject.meshMice-
dc.subject.meshMolecular Sequence Data-
dc.subject.meshMuscle, Skeletal-
dc.subject.meshMyoD Protein-
dc.subject.meshMyoblasts-
dc.subject.meshMyogenin-
dc.subject.meshReceptor, IGF Type 1-
dc.subject.meshReceptors, Tumor Necrosis Factor, Type I-
dc.subject.meshTumor Necrosis Factor-alpha-
dc.titleC2 and C2C12 murine skeletal myoblast models of atrophic and hypertrophic potential: relevance to disease and ageing?en
dc.typeArticleen
dc.contributor.departmentManchester Metropolitan Universityen_GB
dc.identifier.journalJournal of Cellular Physiologyen_GB
All Items in UOBREP are protected by copyright, with all rights reserved, unless otherwise indicated.