Alexandre, from @theglasgowcemi.bsky.social, will share how our team is developing “symbiotic engineered living materials” — 3D constructs where genetically engineered helper cells detect metabolic cues from mesenchymal stem cells and respond by secreting lineage-specific growth factors.

Thanks, I'm happy that you like it😊.
Indeed, another critical component is molecular clutch force loading:

bsky.app/profile/cars...

...can involve also other cell adhesion receptors (e.g., GPI-anchored, such as uPAR, or maybe syndecans, DDRs?) 2/2:

Consistently, some years later (2019), Changede et al. (Sheetz group) showed the existence of integrin nanoclusters bridges build up by activated, but unliganded, integrins. The binding to the thin matrix fibres was mediated by integrins in this case, but it's intriguing to think that this 1/2

I delved even deeper into this a few years later, further highlighting the importance of talin-mediated molecular clutch force loading in this process:

👉 www.sciencedirect.com/science/arti...

This ligand binding-independent integrin signalling was driven by membrane tension. Indeed, the induction of this non-canonical integrin signalling was not restricted to uPAR/vitronectin interaction.
This work introduced the cell membrane as a critical component of the molecular clutch.

This study assessed the possibility of ligand-independent adhesion signalling by integrins, which was a quite controversial hypothesis at the time (maybe still is).
We found that e.g. uPAR-mediated adhesion to vitronectin can induce integrin signalling that does not require integrin ligand binding:

In this work my team and co-workers demonstrated a purely mechanically regulated route for #StemCell #Chondrogenesis via engineering of the hydrogels #viscous nature. No #growthfactors needed. Conducted @uofglasgow.bsky.social @theglasgowcemi.bsky.social Funded @ukri.org