posted on 2021-07-06, 08:29authored byJinfeng Wang, Junyao Li, Juan Liu, Manping Lin, Shilong Mao, Yuanliang Wang, Yanfeng Luo
Osteoblasts actively generate cell
traction force (CTF) to sense
chemical and mechanical microenvironments. Fluid shear stress (FSS)
is a principle mechanical stimulus for bone modeling/remodeling. FSS
and CTF share common interconnected elements for force transmission,
among which the role of the protein-material interfacial force (Fad) remains unclear. Here, we found that, on
the low Fad surface (5.47 ± 1.31
pN/FN), CTF overwhelmed Fad to partially
desorb FN, and FSS exacerbated the desorption, resulting in disassembly
of the actin cytoskeleton and focal adhesions (FAs) to reduce CTF
and establishment of a new mechanical balance at the FN-material interface.
Contrarily, on the high Fad surface (27.68
± 5.24 pN/FN), pure CTF or the combination of CTF and FSS induced
no FN desorption, and FSS promoted assembly of actin cytoskeletons
and disassembly of FAs, regaining new mechanical balance at the cell-FN
interface. These results indicate that Fad is a mechanical regulator for transmission of CTF and FSS, which
has never been reported before.