Graphene oxide activates canonical TGFβ signalling in a human chondrocyte cell line via increased plasma membrane tension
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View abstract on PubMed
Summary
This summary is machine-generated.Graphene oxide (GO) enhances cartilage gene expression by increasing plasma membrane tension, activating mechanosensory pathways and latent TGFβ. This reveals a novel mechanism for GO
Area Of Science
- Biomaterials Science
- Regenerative Medicine
- Cell Signaling
Background
- Graphene oxide (GO) promotes chondrogenesis in 3D scaffolds, but its underlying mechanisms are unclear.
- Understanding GO's chondroinductive effects is crucial for articular cartilage regeneration therapies.
Purpose Of The Study
- To elucidate the effects of GO on the transforming growth factor-beta (TGFβ) signaling pathway in human chondrocytes.
- To identify the specific mechanisms by which GO activates chondrogenic signaling.
Main Methods
- Validation of canonical TGFβ signaling via SMAD-2 phosphorylation and gene expression analysis.
- Utilized a TGFβ signaling reporter assay to determine the onset of GO-induced signal activation.
- Employed fluorescent lifetime imaging (FLIM) and membrane tension probes to assess cell-material interactions in real-time.
Main Results
- Demonstrated GO-induced SMAD-2 phosphorylation and upregulation of TGFβ response genes.
- Identified a novel, real-time increase in plasma membrane tension mediated by GO.
- Revealed activation of mechanosensory pathways and endogenous latent TGFβ in the presence of GO.
Conclusions
- Graphene oxide activates chondrogenic signaling through increased plasma membrane tension and subsequent activation of latent TGFβ.
- Established a novel link between GO, plasma membrane mechanics, and intracellular signaling pathways.
- Provides critical insights into GO's chondroinductive properties for regenerative medicine applications.
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