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Skeletal Mechanobiology
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Alesha B. Castillo, Christopher R. Jacobs
The regulation of osteoclast recruitment and differentiation during remodeling is carried out by a family of tumor necrosis factor (TNF) receptor (TNFR)/TNF-like proteins including the receptor activator of nuclear factor-κB (NF-κB) (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG).11 Osteoblasts and stromal cells enhance bone resorption through the expression of RANKL, a membrane-bound ligand, which binds to RANK on osteoclast precursors12 (Figure 13.1a). Binding activates the expression of osteoclast-specific markers including tartrate-resistant acid phosphatase, cathepsin K (CATK), the calcitonin receptor, and the β3-integrin, and is necessary for osteoclast maturation.12 Mature osteoclasts form a sealing zone and ruffled border atop bone surfaces, and create an acidic environment by releasing H+ ions, CATK, and metalloproteinases, all which serve to degrade bone matrix.13 Osteoblasts can also impede bone resorption through the expression of OPG, a soluble decoy receptor that competitively binds RANKL. Thus, the relative expression of OPG and RANKL in the local environment regulates bone resorption.
Association between polymorphism and haplotype of ATP2B1 gene and skeletal fluorosis in Han population
Published in International Journal of Environmental Health Research, 2023
Yue Gao, Yang Liu, Yuting Jiang, Ming Qin, Zhizhong Guan, Yanhui Gao, Yanmei Yang
The severity of fluorosis does not necessarily rely on the amount of fluoride consumed (Pramanik and Saha 2017), suggesting that other variables influence skeletal fluorosis. It has been reported that genetic variants may contribute to variances in sensitivity or resistance to fluoride exposure among individuals (Kobayashi et al. 2014). Single nucleotide polymorphism (SNP), which underpins variances in disease susceptibility, has been related with individual’s susceptibility to fluorosis. Fluoride exposure has been demonstrated to impact calcium metabolism genes, and single nucleotide polymorphisms in these genes have been linked to fluorosis. The CT/TT genotype at the rs2228570 locus of the vitamin D receptor (VDR) gene was found to be possibly protective against brick tea-type fluorosis in Mongolian subjects aged 46–65 years (Yang et al. 2016). A research of 132 adults in India found gene–gene interactions between rs9340799 and rs2077647 of estrogen receptor 1 (ESR1) and rs1543294 of bone glaprotein (BGLAP) on dental fluorosis. (Chakraborty et al. 2022). An association between fluorosis and Alu I polymorphism in the calcitonin receptor (CTR) gene was revealed in Han Chinese children aged 8–12 years (Jiang et al. 2015).
Chitosan oligosaccharide promotes osteoclast formation by stimulating the activation of MAPK and AKT signaling pathways
Published in Journal of Biomaterials Science, Polymer Edition, 2018
Bing-Li Bai, Zhong-Jie Xie, She-Ji Weng, Zong-Yi Wu, Hang Li, Zhou-Shan Tao, Viraj Boodhun, De-Yi Yan, Zi-Jian Shen, Jia-Hao Tang, Lei Yang
RT-qPCR was utilized to analyze specific gene expression during the formation of osteoclasts. BMMs were plated in 6-well plates at a density of 1x105 cells/well and cultured in complete α-MEM supplemented with 30 ng/ml M-CSF and 50 ng/ml RANKL. Following the RANKL-induced osteoclastogenesis, we treated the cells with different concentrations of COS (0, 5, 50, 500 ng/ml) for 1, 3 or 5 days. Total RNA was isolated from cultured cells using an RNeasy Mini Kit (Qiagen, Valencia, CA, United States) in accordance with the manufacturer’s protocol and Complementary DNA(cDNA) was synthesized from 1 μg of total RNA using reverse transcriptase (TaKaRa Biotechnology, Otsu, Japan). Triplicate PCR reactions were performed using the SYBR Premix Ex Tag Kit (TaKaRa, Biotechnology, Otsu, Japan) and an ABI 7500 Sequencing Detection System (Applied Biosystems, Foster City, CA, USA). Each reaction was run for 40 cycles of: denaturation at 95 °C for 5 s and amplification at 60 °C for 24 s [16]. PCR products were analyzed by electrophoresis in agarose gels and the expression of each gene normalized to the expression of GAPDH. As depicted previously [17], the following mouse primer sets were used: GAPDH, TRAP, nuclear factor of activated T-cells 1(NFATC1), calcitonin receptor(CTR), Cathepsin K(Ctsk), Atp6vo d2, c-fos: GAPDH forward 5′-ACCCAGAAGACTGTGGATGG-3′ and reverse 5′-CACATTGGGGGTAGGAACAC-3′, TRAP forward 5′-CTGGAGTGCACGATGCCAGCGACA-3′ and reverse 5′-TCCGTGCTCGGCGATGGACCAGA-3′, Ctsk forward 5′-CTTCCAATACGTGCAGCAGA-3′ and reverse 5′-TCTTCAGGGCTTTCTCGTTC-3′, Atp6vo d2 forward 5′-ATGGGGCCTTGCAAAAGAAA-3′ and reverse 5′-GCTAACAACCGCAACCCCTC-3′; c-fos forward 5′-CCAGTCAAGAGCATCAGCAA-3′ and reverse 5′-AAGTAGTGCAGCCCGGAGTA-3′, CTR forward 5′-TGCAGACAACTCTTGGTTGG-3′ and reverse 5′-TCGGTTTCTTCTCCTCTGGA-3′, NFATC1 forward 5′-CCGTTGCTTCCAGAAAATAACA-3′ and reverse 5′-TGTGGGATGTGAACTCGGAA-3′.