ArticleMolecular biology reports2000
Glucocorticoid inhibition of C2C12 proliferation rate and differentiation capacity in relation to mRNA levels of the MRF gene family.
Article in Molecular biology reports, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 57 citations in OpenAlex.
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- Gpr18 agonist dampens inflammation, enhances myogenesis, and restores muscle function in models of Duchenne muscular dystrophy.Frontiers in cell and developmental biology · 2023Article
- Influence of COPD systemic environment on the myogenic function of muscle precursor cells in vitro.Respiratory research · 2022Article
- Satellite Cells Exhibit Decreased Numbers and Impaired Functions on Single Myofibers Isolated from Vitamin B6-Deficient Mice.Nutrients · 2021Article
- Resolvin-D2 targets myogenic cells and improves muscle regeneration in Duchenne muscular dystrophy.Nature communications · 2021Article
- Effects of the Combination of β-Hydroxy-β-Methyl Butyrate and R(+) Lipoic Acid in a Cellular Model of Sarcopenia.Molecules (Basel, Switzerland) · 2020Article
- Detecting the Effects of the Glucocorticoid Dexamethasone on Primary Human Skeletal Muscle Cells-Differences to the Murine Cell Line.International journal of molecular sciences · 2020Article
- Protective Effect ofMarine drugs · 2019Article
- Dexamethasone-induced impairment of post-injury skeletal muscle regeneration.BMC veterinary research · 2019Article
- Article
- Cross-talk between the glucocorticoid receptor and MyoD family inhibitor domain-containing protein provides a new mechanism for generating tissue-specific responses to glucocorticoids.The Journal of biological chemistry · 2017Article
- Precocious glucocorticoid exposure reduces skeletal muscle satellite cells in the fetal rat.The Journal of endocrinology · 2017Article
- A novel in vitro model of sarcopenia using BubR1 hypomorphic C2C12 myoblasts.Cytotechnology · 2016Article
- Glucocorticoids and 11β-HSD1 are major regulators of intramyocellular protein metabolism.The Journal of endocrinology · 2016Article
- The effects of stress on brain and adrenal stem cells.Molecular psychiatry · 2016Article
- Effects of eldecalcitol on bone and skeletal muscles in glucocorticoid-treated rats.Journal of bone and mineral metabolism · 2016Article
- mRNA-seq reveals skeletal muscle atrophy in response to handling stress in a marine teleost, the red cusk-eel (Genypterus chilensis).BMC genomics · 2015Article
- The effects of resting and exercise serum from children with cystic fibrosis on C2C12 myoblast proliferation in vitro.Physiological reports · 2014Article
- Inhibition of glycogen synthase kinase-3β attenuates glucocorticoid-induced suppression of myogenic differentiation in vitro.PloS one · 2014Article
- The effects of omega-3 fatty acid supplementation on dexamethasone-induced muscle atrophy.BioMed research international · 2014Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The muscle regulatory factors (MRF) gene family regulate muscle fibre development. Several hormones and drugs also affect muscle development. Glucocorticoids are the only drugs reported to have a beneficial effect on muscle degenerative disorders. We investigated the glucocorticoid-related effects on C2C12 myoblast proliferation rate, morphological differentiation, and subsequent mRNA expression patterns of the MRF genes. C2C12 cells were incubated with the glucocorticoids dexamethasone or alpha-methyl-prednisolone. Both glucocorticoids showed comparable effects. Glucocorticoid treatment of C2C12 cells during the proliferative phase reduced the proliferation rate of the cells dose dependently, especially during the third and fourth day of culture, increased MyoD1, myf-5, and MRF4 mRNA levels, and reduced myogenin mRNA level, compared to untreated control cells. Thus, the mRNA level of proliferation-specific MyoD1 and myf-5 expression does not seem to associate with C2C12 myoblast proliferation rate. Glucocorticoid treatment of C2C12 cells during differentiation reduced the differentiation capacity dose dependently, which is accompanied by a dose dependent reduction of myogenin mRNA level, and increased MyoD1, myf-5, and MRF4 mRNA levels compared to untreated control cells. Therefore, we conclude that glucocorticoid treatment reduces differentiation of C2C12 myoblasts probably through reduction of differentiation-specific myogenin mRNA level, while inducing higher mRNA levels of proliferation-associated MRF genes.
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