Journal
BIOMACROMOLECULES
Volume 22, Issue 8, Pages 3264-3273Publisher
AMER CHEMICAL SOC
DOI: 10.1021/acs.biomac.1c00375
Keywords
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Funding
- National Natural Science Foundation of China [31771013]
- Chongqing University Postgraduates' Innovation Project [CYB15025]
- Visiting Scholar Foundation of Key Laboratory of Biorheological Science and Technology (Chongqing University) [CQKLBST-2018-004]
- Large-scale Instrument and Equipment Open Fund (Chongqing University) [202003150146]
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The protein-material interfacial force (F-ad) plays a crucial role in regulating cell traction force (CTF) and fluid shear stress (FSS) transmission, influencing the structure and function of the actin cytoskeleton and focal adhesions (FAs) within cells, and thereby affecting the mechanical balance between cells and materials.
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 (F-ad) remains unclear. Here, we found that, on the low F-ad surface (5.47 +/- 1.31 pN/FN), CTF overwhelmed F-ad to partially desorb FN, and FSS exacerbated the desorption, resulting in disassembly of the actin cytoskeleton and focal adhesions (FM) to reduce CTF and establishment of a new mechanical balance at the FN-material interface. Contrarily, on the high F-ad 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 F-ad is a mechanical regulator for transmission of CTF and FSS, which has never been reported before.
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