ArticleSkeletal muscle2015
Retinoic acid promotes myogenesis in myoblasts by antagonizing transforming growth factor-beta signaling via C/EBPβ.
Article in Skeletal muscle, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 40 citations in OpenAlex.
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- Chronic alcohol intake elicits distinct multi-omic profiles in the liverbioRxiv : the preprint server for biology · 2025Article
- Vitamin A retinoic acid contributes to muscle stem cell and mitochondrial function loss in old age.JCI insight · 2025Article
- Retinoic acid signalling inhibits myogenesis by blocking MYOD translation in pig skeletal muscle cells.Animal biotechnology · 2024Article
- Aberrant evoked calcium signaling and nAChR cluster morphology in aFrontiers in cell and developmental biology · 2024Article
- Vitamin A injection at birth improves muscle growth in lambs.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2023Article
- Vitamin D3 decreases myoblast fusion during the growth and increases myogenic gene expression during the differentiation phase in muscle satellite cells from Korean native beef cattle.Journal of animal science · 2023Article
- Article
- Effect of All-trans Retinoic Acid on Panniculus Carnosus Muscle Regeneration in Fetal Mouse Wound Healing.Plastic and reconstructive surgery. Global open · 2022Article
- All-trans retinoic acid changes muscle fiber type via increasing GADD34 dependent on MAPK signal.Life science alliance · 2022Article
- All-trans retinoic acid alters the expression of adipogenic genes during the differentiation of bovine intramuscular and subcutaneous adipocytes.Journal of animal science and technology · 2021Article
- miR-206 family is important for mitochondrial and muscle function, but not essential for myogenesis in vitro.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Neutralization of transforming growth factor (TGF)-β1 activity reduced fibrosis and enhanced regeneration of glycerol-injured rat muscle.The Journal of veterinary medical science · 2020Article
- Studying Brown Adipose Tissue in a HumanFrontiers in endocrinology · 2020Review
- All-trans retinoic acid increases the expression of oxidative myosin heavy chain through the PPARδ pathway in bovine muscle cells derived from satellite cells.Journal of animal science · 2018Article
- Neonatal vitamin A injection promotes cattle muscle growth and increases oxidative muscle fibers.Journal of animal science and biotechnology · 2018Article
- CCAAT/enhancer binding protein β is required for satellite cell self-renewal.Skeletal muscle · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe effects of transforming growth factor-beta (TGFβ) are mediated by the transcription factors Smad2 and Smad3. During adult skeletal myogenesis, TGFβ signaling inhibits the differentiation of myoblasts, and this can be reversed by treatment with retinoic acid (RA). In mesenchymal stem cells and preadipocytes, RA treatment can function in a non-classical manner by stimulating the expression of Smad3. Smad3 can bind to and prevent the bzip transcription factor CCAAT/enhancer-binding protein beta (C/EBPβ) from binding DNA response elements in target promoters, thereby affecting cell differentiation. In skeletal muscle, C/EBPβ is highly expressed in satellite cells and myoblasts and is downregulated during differentiation. Persistent expression of C/EBPβ in myoblasts inhibits their differentiation.
methodsUsing both C2C12 myoblasts and primary myoblasts, we examined the regulation of C/EBPβ expression and activity following treatment with TGFβ and RA.
resultsWe demonstrate that treatment with RA upregulates Smad3, but not Smad2 expression in myoblasts, and can partially rescue the block of differentiation induced by TGFβ. RA treatment reduces C/EBPβ occupancy of the Pax7 and Smad2 promoters and decreased their expression. RA also inhibits the TGFβ-mediated phosphorylation of Smad2, which may also contribute to its pro-myogenic activities. TGFβ treatment of C2C12 myoblasts stimulates C/EBPβ expression, which in turn can stimulate Pax7 and Smad2 expression, and inhibits myogenesis. Loss of C/EBPβ expression in myoblasts partially restores differentiation in the presence of TGFβ.
conclusionsTGFβ acts, at least in part, to inhibit myogenesis by upregulating the expression of C/EBPβ, as treatment with RA or loss of C/EBPβ can partially rescue differentiation in TGFβ-treated cells. This work identifies a pro-myogenic role for Smad3, through the inhibition of C/EBPβ's actions in myoblasts, and reveals mechanisms of crosstalk between RA and TGFβ signaling pathways.
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