Bone tissue is remodeled through the catabolic function of the osteoclasts and the anabolic function of the osteoblasts. The process of bone homeostasis and metabolism has been identified to be co‐ordinated with several local and systemic factors, of which mechanical stimulation acts as an important regulator. Very recent studies have shown a mutual effect between bone and other organs, which means bone influences the activity of other organs and is also influenced by other organs and systems of the body, especially the nervous system. With the discovery of neuropeptide (calcitonin gene‐related peptide, vasoactive intestinal peptide, substance P, and neuropeptide Y) and neurotransmitter in bone and the adrenergic receptor observed in osteoclasts and osteoblasts, the function of peripheral nervous system including sympathetic and sensor nerves in bone resorption and its reaction to on osteoclasts and osteoblasts under mechanical stimulus cannot be ignored. Taken together, bone tissue is not only the mechanical transmitter, but as well the receptor of neural system under mechanical loading. This review aims to summarize the relationship among bone, nervous system, and mechanotransduction.
Stem cell-based tissue engineering provides a prospective strategy to bone tissue repair. Bone tissue repair begins at the recruitment and directional movement of stem cells, and ultimately achieved on the directional differentiation of stem cells. The migration and differentiation of stem cells are regulated by nucleoskeletal stiffness. Mechanical properties of lamin A/C contribute to the nucleoskeletal stiffness and consequently to the regulation of cell migration and differentiation. Nuclear lamin A/C determines cell migration through the regulation of nucleoskeletal stiffness and rigidity and involve in nuclear-cytoskeletal coupling. Moreover, lamin A/C is the essential core module regulating stem cell differentiation. The cells with higher migration ability tend to have enhanced differentiation potential, while the optimum amount of lamin A/C in migration and differentiation of MSCs is in conflict. This contrary phenomenon may be the result of mechanical microenvironment modulation.
Backgrounds: Both matrix stiffness and cell morphology have been found as important factors directing MSCs (mesenchymal stem cells) differentiation, but cells also spontaneously adapt their morphology under matrix stiffness stimulation. This study aimed to investigate the interplay of cell morphology and matrix stiffness on osteogenesis and adipogenesis of rBMSCs(rat bone BMSCs) on 2D substrates.Methods and Results: First, we modulated MSCs morphology through different bronectin (FN) concentrations on tissue culture plates (TCPs). We found FN promoted and osteogenesis of BMSCs while suppressing adipogenesis, mediated by FN-induced F-actin polymerization and cell spreading. Based on these ndings, we modulated BMSCs morphology on 0.5 kPa and 32 kPa CytoSoft ® plates through FN concentrations. We found BMSCs on 0.5 kPa substrates coated with 300μg/ml of FN manifested similarly spreading morphology with cells on 32 kPa substrates coated with 100 μg/ml of FN, and cells in both groups dominantly commit osteogenesis. On the other hand, BMSCs on 32 kPa substrates coated with 30μg/ml of FN manifested similarly restricted morphology with cells in on 0.5 kPa substrates with 100μg/ml of FN, and in both groups cells mainly commit adipogenesis. Immuno uorescence staining indicated YAP/TAZ mainly located in cytoplasm when cells exhibited restricted morphology on stiff matrices, while exhibiting signi cant nuclear translocation when cells spread on soft matrices.Conclusions: Cell morphology overrode effects of matrix stiffness on BMSCs differentiation through more robust regulation of YAP/TAZ. Matrix stiffness depended on cell morphology to regulate osteogenesis and adipogenesis of BMSCs.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.