ライフサイエンスコーパス: bone cell

1 of the interaction between crack stress and bone cells.

2 f knowledge related to the biology of NF1 in bone cells.

3 iscuss the mechanisms whereby SCFAs regulate bone cells.

4 gulation of genes expressed in cartilage and bone cells.

5 ulator and effector of mechanical signals in bone cells.

6 teristics were comparable to those of mature bone cells.

7 duced apoptosis in human osteosarcoma U-2 OS bone cells.

8 ectly, via up-regulation of Wnt signaling in bone cells.

9 oordinately with the cell cycle machinery in bone cells.

10 of injury and promoting differentiation into bone cells.

11 gh their syncytial relationship with surface bone cells.

12 otein-5 (IGFBP-5) is abundantly expressed in bone cells.

13 oth of these cancer cell-mediated effects on bone cells.

14 s of OPG in cocultures of myeloma cells with bone cells.

15 tment of both periodontal ligament (PDL) and bone cells.

16 at are operative for the PTH1R in kidney and bone cells.

17 ed any detectable effect on PG metabolism in bone cells.

18 0263 also blocked IL-6 production in primary bone cells.

19 P-4, a potent inhibitor of IGF-II actions in bone cells.

20 rs, C5aR1 and C5aR2, expressed on immune and bone cells.

21 controlling proliferation-related events in bone cells.

22 bone morphogenetic protein-2 (BMP-2) gene in bone cells.

23 r (VDR) and with nuclear extracts from human bone cells.

24 isease arises from changes in the numbers of bone cells.

25 TGF-beta type I receptor on matrix-producing bone cells.

26 nt elongation of primary cilia in IS patient bone cells.

27 e contribute to the development of cancer of bone cells.

28 monal responses within elaborately networked bone cells.

29 nately regulating expression of this gene in bone cells.

30 letion coupled with STAT3 hyperactivation in bone cells.

31 ys and functional dependencies among various bone cells.

32 ls, further substantiating its safety on the bone cells.

33 d bone and serve as an established proxy for bone cells.

34 physiological source of circulating FGF23 is bone cells.

35 ulated Fgf23 in an FGFR1-dependent manner in bone cells.

36 spiratory chain components within individual bone cells.

37 e tissue and breast cancer cells, but not in bone cells.

38 are not fully explained by direct effects on bone cells.

39 hat chondrocytes can directly transform into bone cells.

40 , secrete adipokines, and target neighboring bone cells.

41 s a mediator of nonestrogenic SPI effects on bone cells.

42 lp cells [DPCs]) and alveolar bone (alveolar bone cells [ABCs]) were isolated and separately cocultur

43 Etidronate has specific site and bone cell actions in the periodontium.

44 The impact of bone cell activation on bacterially-induced osteolysis r

45 rties of calcium phosphate (CaP) coatings on bone cell activity and bone-implant osseointegration is

46 PDL) cells communicate stretch to changes in bone cell activity in part via PMD.

47 uency mechanical signals to restore anabolic bone cell activity inhibited by disuse.

48 Whether calcitriol administration affects bone cell activity while PTH is maintained constant shou

49 tic activity, whereas calcimimetic increased bone cell activity.

50 alcimimetics is associated with an increased bone cell activity.

51 ic (nAChRs), but not muscarinic receptors in bone cells, affecting mainly osteoclasts.

52 milar or higher maximum strains than healthy bone cells after short durations of estrogen deficiency

53 orted an intrinsic self-defense mechanism of bone cells against breast cancer cells: a critical role

54 anical forces into pro-survival signaling in bone cells, albeit in a ligand-independent manner.

55 Osteocytes are the most abundant type of bone cell and play crucial roles in bone health.

56 mbedded osteocytes comprise more than 95% of bone cells and are major regulators of osteoclast and os

57 regulated communication between matrix-bound bone cells and BM-MSPCs, which dictates bone formation a

58 CXCR4(+) pericytes, which differentiate into bone cells and contribute to bone and hematopoietic rege

59 ignaling may provide potent cross-talk among bone cells and endothelial cells that is essential for f

60 t mediate signaling within their neighboring bone cells and in distant tissues.

61 e of fractalkine from the plasma membrane of bone cells and its action is reversed by nilutamide--an

62 e interactions between the immune system and bone cells and may open new therapeutic avenues in modul

63 likely disrupt the mechanical environment of bone cells and may thereby initiate a mechanobiological

64 h those reported for MGP; OC was detected in bone cells and mineralized structures but also in soft a

65 understanding of how glucocorticoids affect bone cells and novel ways of prevention.

66 Finally, GPC-1 was expressed in mouse tibia bone cells and present during bone loss induced by mouse

67 orylation levels in human and mouse cultured bone cells and regulates gene expression patterns in a P

68 The model comprises human bone cells and secreted extracellular matrix (ECM); howe

69 nically induced release of prostaglandins by bone cells and subsequent osteogenesis.

70 between cells of the bone marrow and between bone cells and the brain through which bone is constantl

71 l effect on the behavior of both myeloma and bone cells and therefore may represent one of the centra

72 ese Vdr gene enhancers in mesenchyme-derived bone cells and to describe the epigenetic histone landsc

73 bmicrometre-sized channels that interconnect bone cells and vascular canals--and the collagen fibre b

74 ressed in those tissues and in skin, kidney, bone cells, and (probably) in liver and muscle.

75 nteractions of MGUS cells with immune cells, bone cells, and others in the bone marrow niche may be k

76 the most abundant growth factors secreted by bone cells, and regulation of TGF-beta expression is cru

77 one histomorphometry, and by measurements of bone cell apoptosis.

78 , the C-terminal region of PTH, by promoting bone-cell apoptosis, may be important in opposing the an

79 Bone cells are also sensitive to the chemical products g

80 nstrated that many, perhaps the majority, of bone cells are derived via direct transformation from ch

81 Bone cells are exposed to dynamic mechanical stimulation

82 environment but the widely held concept that bone cells are programmed to respond to local mechanical

83 However, the mechanisms of ATF4 in bone cells are still not clear.

84 It resembles skeletal osteogenesis, and many bone cells as well as bone-related factors involved in b

85 fixation, but also support the functions of bone cells, as clinically required for craniomaxillofaci

86 and a mixed agonist/antagonist profile in a bone cell assay versus a breast cancer assay.

87 ing to consensus elements, are maintained in bone cells at different stages of differentiation.

88 nt protein transgenic mouse lines to isolate bone cells at distinct stages of osteoprogenitor maturat

89 rough osseointegration, the process in which bone cells attach to an artificial surface without forma

90 The bone phenotype was analyzed in vivo, and bone cell behavior was analyzed ex vivo.

91 ere were minimal differences in bone mass or bone cells between PAR1 KO and WT mice.

92 nxs are expressed in bone, but their role in bone cell biology is not completely understood.

93 omewide association meta-analysis studies in bone cell biology.

94 s biochemical and transcriptional changes in bone cells by an unknown mechanism.

95 cause sex steroids regulate the life span of bone cells by modulating cytoplasmic kinase activity via

96 ing among conventional membrane receptors on bone cells can vary with hormone or growth factor treatm

97 (3D) myeloma BM coculture model that mimics bone cell/cancer cell interactions within the bone micro

98 However, how bone cells communicate with BM-MSPCs to coordinate bone

99 The inherent heterogeneity of bone cells complicates the interpretation of microarray

100 Bone cells controlling bone remodeling (i.e. osteoblasts

101 e marrow, therefore haematopoietic cells and bone cells could be extrinsic factors for each other.

102 ed to analyze bone parameters, apoptosis and bone cell counts, and expression of bone remodeling mark

103 of metastatic breast cancer cells to invade bone cell cultures and suppresses their ability to form

104 Bone cell cultures secreted osteocalcin (OC) and did not

105 Bone cell cultures were established using explants obtai

106 of macrophages/osteoclast progenitors in the bone cell cultures, as assessed by mRNA and protein expr

107 Our key finding is that BMP2 controls bone cell determination by inducing miRNAs that target m

108 s cellular processes, but its involvement in bone cell development and homeostasis is not yet clear.

109 s a novel mechanism underlying adipocyte and bone cell development.

110 However, the role of Hem1 in bone cell differentiation and bone remodeling is unknown

111 n TGF-betaRI levels that parallel changes in bone cell differentiation or activity.

112 on of swimming unicellular organisms, alters bone cell differentiation, and modifies gene expression

113 thway has been shown to play a major role in bone cell differentiation, proliferation and apoptosis.

114 and during the early proliferative stages of bone cell differentiation.

115 nd is a potent modulator of osteogenesis and bone cell differentiation.

116 ys, the 3D dynamic flow environment affected bone cell distribution and enhanced cell phenotypic expr

117 ible genetic fate mapping confirmed that new bone cells do not arise from dedifferentiated osteoblast

118 xacerbated COX2/NLRP3/IL-1beta activation in bone cells during bone remodeling under estrogen deficie

119 ilage in long bones, directly transform into bone cells during endochondral bone formation.

120 ght be involved in the responses of alveolar bone cells during orthodontic tooth movement.

121 Osteocytes, the bone cells embedded in the mineralized matrix, control b

122 the vitamin D receptor, and new factors for bone cell embryogenesis and function as a way of introdu

123 ice, we confirmed the functionality of these bone cell enhancers in vivo as well as in vitro.

124 fic skeletal compartments through effects on bone cells, enhancing osteoblast activity but inhibiting

125 erials to guide differentiation of MSCs into bone cells ensuring complete bone regeneration.

126 trafficking is critical for the function of bone cells, exemplified by bone diseases such as osteope

127 hese findings suggest that breast cancer and bone cells exhibit differential responses to treatment w

128 ost interestingly, we show that osteoporotic bone cells experience similar or higher maximum strains

129 of titanium dioxide nanoparticles on primary bone cells, exploring the events occurring at the nano-b

130 d provide further insight into how GCs alter bone cell fate.

131 ence and expansion of distinct cartilage and bone cell fates in an invariant temporal and spatial pat

132 myriad of blood vessels, tissue surfaces and bone cells for bacterial colonization.

133 ent to induce osteoblast differentiation and bone cell formation.

134 ytes, consistent with findings using primary bone cells from newborn mouse calvaria.

135 Bone cells from OA patients can influence cartilage meta

136 s celastrol, BMS-345541, and parthenolide on bone cell function in vitro and ovariectomy-induced bone

137 Elucidating the effect of Pb on bone cell function is therefore critical for understandi

138 emonstrate that SSRIs differentially inhibit bone cell function via apoptosis.

139 , could play an important role in modulating bone cell function.

140 f loosening due to debris-induced changes in bone cell function.

141 a better understanding of the regulators of bone cell function.

142 ge, related to the effects of excess cAMP on bone cell function.

143 r more central transcriptional regulators of bone cell gene expression.

144 echanisms that are requisite for fidelity of bone cell growth and differentiation, as well as for ske

145 irect role in early skeletal development and bone cell growth and proliferation.

146 IGFBP-5 stimulates bone cell growth, and its inhibition by glucocorticoids

147 role(s) of endogenous IGFBP-5 in regulating bone cell growth, differentiation, and survival, we used

148 en receptor (AR) is critical in both PCa and bone cell growth.

149 s whole-body homoeostasis through actions on bone cells, haematopoietic stem cells and extra-medullar

150 To date, the direct impact of C. acnes on bone cells has never been explored.

151 the effects of varying doses of MTX on mouse bone cells in culture.

152 there was no significant difference between bone cells in healthy and osteoporotic bone.

153 due to the altered and aberrant functions of bone cells in hyperglycemic conditions.

154 em cells (MSCs) from myeloma patients and in bone cells in myelomatous bones was lower than in health

155 t cell transformation from chondrocytes into bone cells in postnatal bone growth.

156 rtrophic chondrocytes contributed to ~80% of bone cells in subchondral bone, ~70% in a somewhat more

157 the investigation of molecular signaling in bone cells in their 3D environment and could be applied

158 terstitial oscillatory fluid flow (OFF), and bone cells in vitro respond to mechanical loading.

159 o characterize the mechanical environment of bone cells in vivo, and the mechanical environment of os

160 e direct transformation of chondrocytes into bone cells in vivo.

161 rin alpha, meltrin beta, mdc9, and mdc15) in bone cells, including osteoclasts and osteoblasts.

162 nslate fluid flow into cellular responses in bone cells independently of Ca(2+) flux and stretch-acti

163 lpha to facilitate formation of multinuclear bone cells indicates a possible role in periodontitis-as

164 al of the current study was to determine how bone cells integrate signals from the GH/IGF-1 to enhanc

165 Tumor-bone cell interactions are critical for the development

166 on prostate cancer cells and prostate cancer/bone cell interactions in vitro and in vivo.

167 l characteristic features of HPO4(2-) at the bone-cell interface.

168 The true biological environment of a bone cell is thus derived from a dynamic interaction bet

169 ver that a 'track' of tissue prone to become bone cells is a previously undescribed ligament.

170 s suggest that the mechanical environment of bone cells is altered during early-stage osteoporosis, a

171 e direct transformation of chondrocytes into bone cells is common in both long bone and mandibular co

172 However, its mechanism of action in bone cells is largely unknown.

173 However, its mechanism of action on bone cells is largely unknown.

174 d the mechanical environment of osteoporotic bone cells is not known.

175 We hypothesized that Klotho in bone cells is part of an autocrine feedback loop that re

176 n to mechanistic in vitro studies of primary bone cells is providing additional insight into the mech

177 itamin D receptor (VDR), whose expression in bone cells is regulated positively by 1,25(OH)2D3, retin

178 e in COX-2 mRNA expression levels in primary bone cells isolated from AC6 knockout mice compared to c

179 ral details, including the cement sheath and bone cell lacunae of the selected bone trabecula.

180 ion, cystinosin deficiency primarily affects bone cells, leading to a bone loss phenotype of KO mice,

181 ssion profiling of total RNA from ten normal bone cell lines and eleven OGS-derived cell lines by mic

182 K (extracellular signal-regulated kinase) in bone cell lines.

183 6(tdTomato) (tracing marker), 2.3 Col1(GFP) (bone cell marker), and aggrecan Cre(ERT2) (onetime tamox

184 est that increasing LRP5 signaling in mature bone cells may be a strategy for treating human disorder

185 ifferentiated cell comprising 90%-95% of all bone cells, may have multiple functions, including actin

186 luence the postnatal skeleton, the impact of bone cell mechano-transduction on early skeletal develop

187 sitive ion channel involved in cartilage and bone cell mechanosensing, mutations of which lead to ske

188 olecular mechanism linking primary cilia and bone cell mechanotransduction that involves adenylyl cyc

189 otent physical stimulus in the regulation of bone cell metabolism.

190 ysical signal for loading-induced changes in bone cell metabolism.

191 mproved bone health by reducing PCa-mediated bone cell modulation.

192 ignaling between MLO-Y4 cells in a connected bone cell network.

193 Generating 3D bone cell networks in vitro that mimic the dynamic proce

194 drogel to efficiently differentiate 3D human bone cell networks, facilitating future in vitro studies

195 s containing the aforesaid DNA fragments and bone cell nuclear extract resulted in further retardatio

196 esting that syndecan's effect on myeloma and bone cells occurs through different mechanisms.

197 determined for PGs derived from normal human bone cells of 14 donors (age range, fetal to 60 years).

198 ssays reveal the adherence and growth of new bone cells on the material.

199 e regeneration strategies involve culture of bone cells on various biomaterial scaffolds, which are o

200 the effect of osteocytes, a mechanosensitive bone cell, on the migratory behavior of tumor cells.

201 that alterations in TGF-beta 2 synthesis by bone cells, or in their responsiveness to TGF-beta 2, ma

202 It has become increasingly clear that bone cells, osteoblasts, osteoclasts, and osteocytes, co

203 Whether PPARgamma expression in bone cells, particularly osteocytes, regulates energy me

204 ate SAMs induce differentiation of hMSC to a bone cell phenotype and promote bone formation on modifi

205 l cycle and activating genes that facilitate bone cell phenotype development.

206 Mechanotransduction in bone cells plays a pivotal role in osteoblast differenti

207 on patterns from unsorted or isolated sorted bone cell populations at days 7 and 17 of calvarial cult

208 entify and test various hypotheses regarding bone cell populations dynamics.

209 on up to 5.6-fold when osteoclast-containing bone cell populations from neonatal rats were cultured f

210 ther ailments may have unintended effects on bone cell populations.

211 Here we report that bone cells possess primary cilia that project from the c

212 Fluoride's actions on bone cells predominate as anabolic effects both in vitro

213 erleukin-1 beta (an amplifier of stromal and bone cell production of interleukin-6), and serum solubl

214 ion factors participate in the regulation of bone cell proliferation and differentiation.

215 se restriction state" it induces and impacts bone cell proliferation and differentiation.

216 ressed directly the contribution of Runx2 to bone cell proliferation using calvarial osteoblasts from

217 We showed a direct impact of C. acnes on bone cells, providing new explanations about the develop

218 gen is established to have direct effects on bone cells, recent animal studies have identified additi

219 nment at the cellular level, the forces that bone cells recognize, and the integrated cellular respon

220 e metabolism, could have opposite actions on bone cells regulating expression of cytokine receptor ac

221 combining ATP and parathyroid hormone, a key bone cell regulator.

222 Alternatively, we observed that bone cells remain unaffected by the treatment of R. cren

223 is essential for somatic growth and promotes bone cell replication and differentiation.

224 central role in skeletal growth by promoting bone cell replication and differentiation.

225 in promoting skeletal growth by stimulating bone cell replication and differentiation.

226 a key role in skeletal growth by stimulating bone cell replication and differentiation.

227 key role in skeletal growth and can enhance bone cell replication and differentiation.

228 Moreover, FGF23-treated bone cells required Klotho to increase FGF23 mRNA and ER

229 ex process, as the functional development of bone cells requires that regulatory signals be temporall

230 dies offer a glimpse into how these critical bone cells respond to mechanical load in vivo, as well a

231 Bone cells respond to the integrated effects of local an

232 erentiation and survival of osteoclasts, the bone cells responsible for the resorption of mineralized

233 Among bone cells, sclerostin is found nearly exclusively in th

234 However, the mechanisms by which bone cells sense mechanical forces, resulting in increas

235 vel bayesian comparative method to show that bone-cell size correlates well with genome size in extan

236 The adult zebrafish caudal fin, and bone cells specifically, have been crucial for the under

237 In turn, bone cell spheroid formation results in the up-regulatio

238 of three-dimensional cellular condensations (bone cell spheroids) within 24 to 48 hours.

239 ave revealed that, apart from T and B cells, bone cells such as osteoclasts and innate immunity cells

240 Seven cytokines were measured in OA bone cell supernatants.

241 modify the amount of TbetaRII protein on the bone cell surface.

242 portant for nanoparticle internalization and bone cells survival.

243 , pancreas, spleen, skin, vena cava, marrow, bone (cells), tendon (Achilles), ligament (anterior cruc

244 l, these treatments have specific effects on bone cells that are independent of the PTH level.

245 s it fails to phosphorylate p38 MAPK in U2OS bone cells that are stably transfected with AR.

246 In this study, we describe adult mouse bone cells that exhibit several features characteristic

247 Osteocytes are bone cells that form cellular networks that sense mechan

248 to have a direct effect on FGF23 release by bone cells that, in turn, causes renal phosphate excreti

249 mechanical function and shape of bones, the bone cells, the matrix they produce, and the mineral tha

250 of FRZB/sFRP3 mRNA in OGS cells compared to bone cells; this down-regulation of Frzb/sFRP3 mRNA expr

251 a play a role in mediating mechanosensing in bone cells through an unknown mechanism that does not in

252 Taken together, these results indicate that bone cells, through local glucocorticoid signalling, are

253 rosis, may affect the birth or death rate of bone cells, thus reducing their numbers.

254 highlights molecular aberrations that cause bone cells to become dysfunctional, as well as therapeut

255 ossible that porins could also interact with bone cells to cause aberrant bone remodeling and that th

256 cretion of prometastatic factors that act on bone cells to change the skeletal microenvironment.

257 ollagenolytic enzyme, enabling cartilage and bone cells to cleave high-density fibrillar collagen and

258 f lineage progression of chondrocyte-derived bone cells to form osteoblasts and osteocytes in metaphy

259 es have demonstrated that insulin stimulates bone cells to produce and activate osteocalcin, an endoc

260 nd its homeostasis depends on the ability of bone cells to sense and respond to mechanical stimuli.

261 pathways that constitute early responses of bone cells to strain.

262 e in these cells, thereby maintaining normal bone-cell turnover.

263 Osteoblasts were the principal bone cell type expressing MCP-1.

264 ing analysis, revealing that only one of the bone cell-type enhancers bound VDR in kidney tissue, and

265 nes are selectively expressed in a subset of bone cell types during differentiation.

266 results provide a framework for identifying bone cell types in murine single-cell RNA-seq datasets a

267 actions on human osteoclasts (OCs) and other bone cell types.

268 ver, expression profiles of these factors in bone cells under diabetes mellitus (DM) and estrogen-def

269 ence that extracellular ATP acts directly on bone cells via P2 receptors.

270 synchrotron X-ray tomography to measure the bone cell volumes, which correlate with genome size in l

271 the donor origin of the fully differentiated bone cells was proven using species-specific probes.

272 encoding Wnt receptors in mouse tissues and bone cells we identified Frizzled 8 (Fzd8) as a candidat

273 iling of prostate cancer cells cultured with bone cells, we demonstrate the changing energy requireme

274 tor G-coupled protein receptor 40 (GPR40) in bone cells, we hypothesized that this receptor may play

275 unction with in situ expression profiling in bone cells, we identified bone lining cells as important

276 e the mechanisms of strain responsiveness in bone cells, we investigated in vitro the responses of pr

277 Mouse calvarial bone cells were cultured in media containing ATRA, with

278 Primary alveolar bone cells were exposed to the SASP via in vitro senesce

279 In contrast, less differentiated bone cells were less sensitive to ligand-dependent recep

280 Osteocytes, the most abundant bone cells, were shown to orchestrate bone modeling duri

281 provides a physical link between loading and bone cells, where mechanoreceptors, such as integrins, i

282 Our data indicates defective cilia in IS bone cells, which may be linked to heterogeneous gene va

283 Treatment of bone cells with an inhibitory anti-rat interstitial coll

284 ing the remodeling of bone, communication of bone cells with cells of other lineages, crosstalk betwe

285 Infection of bone cells with RRV was validated using an established R

286 While the interaction of bone cells with their mechanical environment is complex,