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Calcium-Collagen Coupling is Vital for Biomineralization Schedule.

ABSTRACT: Biomineralization is a chemical reaction that occurs in organisms in which collagen initiates and guides the growth and crystallization of matched apatite minerals. However, there is little known about the demand pattern for calcium salts and collagen needed by biomineralization. In this study, natural bone biomineralization is analyzed, and a novel interplay between calcium concentration and collagen production is observed. Any quantitative change in one of the entities causes a corresponding change in the other. Translocation-associated membrane protein 2 (TRAM2) is identified as an intermediate factor whose silencing disrupts this relationship and causes poor mineralization. TRAM2 directly interacts with the sarcoplasmic/endoplasmic reticulum calcium ATPase 2b (SERCA2b) and modulates SERCA2b activity to couple calcium enrichment with collagen biosynthesis. Collectively, these findings indicate that osteoblasts can independently and directly regulate the process of biomineralization via this coupling. This knowledge has significant implications for the developmentally inspired design of biomaterials for bone regenerative applications.

SUBMITTER: Zhang J

PROVIDER: S-EPMC8336496 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Biomineralization is the process by which organisms use minerals to harden their tissues and provide them with physical support. Biomineralizing cells concentrate the mineral in vesicles that they secret into a dedicated compartment where crystallization occurs. The dynamics of vesicle motion and the molecular mechanisms that control it, are not well understood. Sea urchin larval skeletogenesis provides an excellent platform for investigating the kinetics of mineral-bearing vesicles. Here we used lattice light-sheet microscopy to study the three-dimensional (3D) dynamics of calcium-bearing vesicles in the cells of normal sea urchin embryos and of embryos where skeletogenesis is blocked through the inhibition of Vascular Endothelial Growth Factor Receptor (VEGFR). We developed computational tools for displaying 3D-volumetric movies and for automatically quantifying vesicle dynamics. Our findings imply that calcium vesicles perform an active diffusion motion in both, calcifying (skeletogenic) and non-calcifying (ectodermal) cells of the embryo. The diffusion coefficient and vesicle speed are larger in the mesenchymal skeletogenic cells compared to the epithelial ectodermal cells. These differences are possibly due to the distinct mechanical properties of the two tissues, demonstrated by the enhanced f-actin accumulation and myosinII activity in the ectodermal cells compared to the skeletogenic cells. Vesicle motion is not directed toward the biomineralization compartment, but the vesicles slow down when they approach it, and probably bind for mineral deposition. VEGFR inhibition leads to an increase of vesicle volume but hardly changes vesicle kinetics and doesn't affect f-actin accumulation and myosinII activity. Thus, calcium vesicles perform an active diffusion motion in the cells of the sea urchin embryo, with diffusion length and speed that inversely correlate with the strength of the actomyosin network. Overall, our studies provide an unprecedented view of calcium vesicle 3D-dynamics and point toward cytoskeleton remodeling as an important effector of the motion of mineral-bearing vesicles.

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Calcium-Collagen Coupling is Vital for Biomineralization Schedule.

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