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Myoblasts Isolated from Hypertrophy-Responsive Callipyge Muscles Show Altered Growth Rates and Increased Resistance to Serum Deprivation-Induced Apoptosis
- Source :
- Cells Tissues Organs. 187:141-151
- Publication Year :
- 2007
- Publisher :
- S. Karger AG, 2007.
-
Abstract
- Back and hind limb muscles of sheep paternally heterozygous for the callipyge single nucleotide polymorphism undergo extensive hypertrophy shortly after birth. We have established cell cultures from foetal semitendinosus and longissimus dorsi muscles of normal and callipyge animals. Cultures were assessed for rates of proliferation, cell death, myogenicity and DLK1 expression. Myoblasts from callipyge semitendinosus, but not longissimus dorsi muscles, proliferated faster than myoblasts isolated from normal semitendinosus muscle, and cells isolated from either callipyge muscle were more resistant to serum deprivation-induced apoptosis than equivalent cells isolated from normal individuals. Theseobservations indicate that there are intrinsic differences in the behaviour of isolated myoblasts, which are associated with their muscle and genotype of origin. As myoblasts are the cells responsible for hypertrophy of muscle fibres, the observed differences in cell growth may play a role in the hypertrophy of certain muscles in callipyge animals.
- Subjects :
- Male
medicine.medical_specialty
Histology
Cell Survival
Sheep Diseases
Apoptosis
Gestational Age
Complement factor I
Hindlimb
Biology
Culture Media, Serum-Free
Muscle hypertrophy
Fetal Development
Myoblasts
Muscular Diseases
Internal medicine
medicine
Animals
Myocyte
Muscle, Skeletal
Cells, Cultured
Sheep, Domestic
Cell Proliferation
Cell growth
Skeletal muscle
Hypertrophy
Flow Cytometry
Polar overdominance
Endocrinology
medicine.anatomical_structure
Female
Anatomy
Subjects
Details
- ISSN :
- 14226421 and 14226405
- Volume :
- 187
- Database :
- OpenAIRE
- Journal :
- Cells Tissues Organs
- Accession number :
- edsair.doi.dedup.....6e2e0c5a3e7698df45b90180b8867fdf
- Full Text :
- https://doi.org/10.1159/000110080