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Differences in bone formation through the different techniques are covered.
Histological analysis of the in vivo samples revealed extensive new bone formation through the remodeling of the cartilage template.
Osteoblasts are responsible not only for bone formation, through the secretion of collagen type I, but also for sensing the mechanical stimuli due to bone surface strain.
We showed that Zfp467 binds to and regulates the expression of the SOST gene, which encodes a secreted glycoprotein named sclerostin (Sost) that is expressed exclusively by osteocytes and functions as a negative regulator of bone formation through the modulation of Wnt signaling.
Furthermore, luciferase reporter assay, Western blotting, enzyme-linked immunosorbent assay (ELISA), and immunofluorescence showed that Si(OH 4 decreased TNFα-induced activation of NF-κB, a signal transduction pathway that inhibits osteoblastic bone formation, through the known miR-146a negative feedback loop.
Thus, cross-talk between Pkd1 and Kif3a may play a counterbalancing role on bone formation through the differential regulation of ostoegenesis and adipogenesis in bone.
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A variety of bone metabolism factors regulate bone formation through this axis.
Endogenous Wnt signaling plays an important role in bone formation through stimulating the osteoblastogenesis and suppressing the adipogenesis and osteoclastogenesis.
The results presented in vivo and in vitro study demonstrated that the SCPP could accelerate bone formation through stimulating the secretion of VEGF and bFGF from osteoblasts, making it attractive for bone regeneration.
Additionally, anti-miR-222 enhanced in vivo ectopic bone formation through targeting the cell-cycle inhibitor CDKN1B (cyclin-dependent kinase inhibitor 1B).
BMPs are responsible for the stimulation of bone formation through binding to the activin receptor type 1 (encoded by the AVCR1 gene receptor), a BMP type 1 receptor.
More suggestions(16)
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bone cement through the
bone destruction through the
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