Tatsuhisa Yuasa's research while affiliated with Meikai University and other places
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Publications (6)
Estrogen deficiency causes bone loss, which can be prevented by estrogen replacement therapy. Using a recently developed technique for isolation of highly purified mammalian osteoclasts, we showed that 17 beta-estradiol (E2) was able to directly inhibit osteoclastic bone resorption. At concentrations effective for inhibiting bone resorption, E2 als...
To address the relation between osteoblast growth and cell-to-cell communication, we examined the effects of basic fibroblast growth factor (bFGF) and 12-O-tetradecanoylphorbol-13-acetate (TPA), both potent stimulators of osteoblastic proliferation, on gap junctional intercellular communication between osteoblastic MC3T3-E1 cells. The level of inte...
The decrease in estrogen levels that follows the onsot of menopause causes rapid bone loss, resulting in osteoporosis. However, the mechanism by whicli this occurs remains unclear, especially concerning the regulation of osteodasts, i.e., the bone-resorbing cells. Using a pit assay (bone-resorbing assay) involving isolated mature-osteoclasts from r...
When unfractionated rabbit bone cells were seeded and incubated on a collagen gel, tartrate-resistant acid phosphatase (TRAP)-positive multinucleate cells (MNCs) adhered to the surface of the collagen gel more readily than other types of cells. Based on the differences in adherence of the MNCs onto the collagen gel, we developed a new method for th...
The decrease in estrogen levels that follows the onset of menopause causes rapid bone loss, resulting in osteoporosis. However, the mechanism by which this occurs remains unclear, especially concerning the regulation of osteoclasts, i.e. the bone-resorbing cells. Using a pit assay involving isolated mature osteoclasts from rabbit long bones, we fou...
In contrast to vitamin K1(VK1), vitamin K2(VK2) inhibited osteoclastic bone resorption by unfractionated bone cells and isolated osteoclasts. To investigate the mechanism of inhibition of osteoclastic bone resorption by VK2, we examined the effect of this vitamin on osteoclast apoptosis using a DNA-binding fluorescent dye, Hoechst 33258. In unfract...
Citations
... Isolation of osteoclasts. Isolation of osteoclasts was performed from long bones as previously described 43 . ...
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... Vitamin K also plays a significant role in bone health by regulating bone mineralization through the inhibition of osteoclast activity and bone resorption (Kameda et al., 1996;Sugiyama and Kawai, 2001). Moreover, research indicates a reduction in vitamin K levels within astronauts' bodies during spaceflight (Smith et al., 2005). ...
... On the other hand, the physiological inhibitors of osteoclast differentiation and activation, such as osteoprotegerin (OPG), can also directly suppress CatK expression [32]. Among the inhibitors of CatK mRNA expression are estrogen [32], Interferon-γ (INF-γ), IL-10, -12, and -18 while IL-1α, -6, -11, -15, and -17 stimulate CatK expression in osteoclasts [33][34][35]. The negative effect of estrogens on osteoclasts is mediated by a membrane receptor inducing a phosphorylation cascade of various proteins, including Src. ...
... Fibroblast growth factor (FGF)-23 and estrogen are hormones derived mainly from the bone and ovaries (testes in males), respectively, and are important regulators of bone metabolism and cardiovascular outcomes (Lu & Hu, 2017;Quarles, 2012). Whereas inflammation, directly and indirectly, increases phosphaturic FGF23 (Francis & David, 2016), an anti-inflammatory role has been mainly attributed to estrogen (Chakrabarti et al., 2008;Josefsson et al., 1992), a hormone that prevents bone loss (Kameda et al., 1997;Nakamura et al., 2007) and reduces vascular injuries and atherosclerosis (Arnal et al., 2010;Meng et al., 2021;Xing et al., 2009). Egli-Spichtig et al. (2019 reported increased serum intact FGF23 (iFGF23) in IL-10 KO mice at 12-14 weeks of age. ...
... 138 Conversely, FGF-2 applied from 8-24 h induced a reduction in Cx43 protein levels and intercellular dye transfer in MC3T3-E1 osteoblastic cells. 139 Short-term (r30 min) treatment of these cells with FGF-2 induced a transient association of Cx43 with activated PKC-d at the plasma membrane, and a significant increase in Cx43 phosphorylation at serine 368. 140 It is interesting to note that Cx43 could modulate the response of osteoblasts to FGF-2, since overexpression of Cx43 increased the transcriptional response of osteocalcin in MC3T3-E1 osteoblasts, which is an effect that also depended on PKC-d activation. ...
