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Transforming growth factor-beta1-induced satellite cell apoptosis in chickens is associated with beta1
X Li1, D C McFarland, S G Velleman
1Department of Animal Sciences, The Ohio State University, Wooster, OH 44691, USA.
Abstract:
Transforming growth factor-beta1 (TGF-beta1) induces apoptosis in many types of cells. The cell adhesion receptor, beta1 integrin subunit, prevents apoptosis and may be involved in TGF-beta1-induced muscle cell apoptosis. In the current study, chicken primary satellite cells, myogenic precursors, were used to investigate the apoptotic effect of TGF-beta1 on muscle cells. The data from the current study showed that the addition of exogenous TGF-beta1 reduced beta1 integrin expression and altered its localization. Treatment of the satellite cells with TGF-beta1 increased the number of apoptotic cells indicated by annexin-V using flow cytometry. The number of caspase-positive cells was increased in the TGF-beta1-treated immunostained cells, which supported that TGF-beta1 induced satellite cell apoptosis. It has been shown that beta1 integrin is involved in muscle cell survival. In response to the activation of beta1 integrin, focal adhesion kinase (FAK) phosphorylates tyrosine at residue 397 and activates cell survival signal transduction. The phosphorylation of FAK was significantly reduced from 30 min to 4 h after TGF-beta1 treatment during both satellite cell proliferation and differentiation. These data suggested that the apoptotic effect of TGF-beta1 on satellite cells is likely associated with a beta1 integrin-mediated FAK signaling pathway during satellite cell proliferation and differentiation.
Insights
Transforming growth factor-beta1 (TGF-beta1) induces apoptosis in chicken muscle cells by reducing beta1 integrin expression. This process involves the beta1 integrin-mediated focal adhesion kinase (FAK) signaling pathway, impacting cell survival.
Area of Science:
- Muscle cell biology
- Cell signaling pathways
- Apoptosis research
Background:
- Transforming growth factor-beta1 (TGF-beta1) is known to induce apoptosis across various cell types.
- The beta1 integrin subunit, a cell adhesion receptor, plays a role in preventing apoptosis and may influence TGF-beta1-induced muscle cell death.
Purpose of the Study:
- To investigate the apoptotic effects of TGF-beta1 on chicken primary satellite cells (muscle precursors).
- To explore the involvement of beta1 integrin and focal adhesion kinase (FAK) signaling in TGF-beta1-induced muscle cell apoptosis.
Main Methods:
- Primary chicken satellite cells were treated with exogenous TGF-beta1.
- Beta1 integrin expression and localization were analyzed.
- Apoptosis was quantified using annexin-V staining and flow cytometry.
- Caspase activation was assessed via immunostaining.
- Focal adhesion kinase (FAK) phosphorylation at tyrosine 397 was measured over time.
Main Results:
- Exogenous TGF-beta1 treatment reduced beta1 integrin expression and altered its cellular localization.
- TGF-beta1 significantly increased the number of apoptotic satellite cells and caspase-positive cells.
- The phosphorylation of FAK at residue 397 was markedly decreased following TGF-beta1 treatment during both proliferation and differentiation phases.
- These changes suggest TGF-beta1 inhibits the pro-survival signaling initiated by beta1 integrin activation.
Conclusions:
- TGF-beta1 induces apoptosis in chicken muscle satellite cells.
- The apoptotic effect is linked to the downregulation of beta1 integrin expression and activity.
- TGF-beta1-induced apoptosis in satellite cells is mediated through a beta1 integrin-dependent FAK signaling pathway during proliferation and differentiation.
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