ライフサイエンスコーパス: bone cell

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

2 teristics were comparable to those of mature bone cells.

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

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

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

6 oordinately with the cell cycle machinery in bone cells.

7 gh their syncytial relationship with surface bone cells.

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

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

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

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

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

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

14 spiratory chain components within individual bone cells.

15 0263 also blocked IL-6 production in primary bone cells.

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

17 controlling proliferation-related events in bone cells.

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

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

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

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

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

23 monal responses within elaborately networked bone cells.

24 nately regulating expression of this gene in bone cells.

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

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

27 hat chondrocytes can directly transform into bone cells.

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

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

30 gulation of genes expressed in cartilage and bone cells.

31 ulator and effector of mechanical signals in bone cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 Bone cells are also sensitive to the chemical products g

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

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

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

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

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

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

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

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

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

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

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

71 (3D) myeloma BM coculture model that mimics bone cell/cancer cell interactions within the bone micro

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

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

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

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

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

77 Bone cell cultures were established using explants obtai

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 ent to induce osteoblast differentiation and bone cell formation.

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

101 Bone cells from OA patients can influence cartilage meta

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 Tumor-bone cell interactions are critical for the development

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 6(tdTomato) (tracing marker), 2.3 Col1(GFP) (bone cell marker), and aggrecan Cre(ERT2) (onetime tamox

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 Bone cells respond to the integrated effects of local an

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

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

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

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

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

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

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

189 Seven cytokines were measured in OA bone cell supernatants.

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

191 portant for nanoparticle internalization and bone cells survival.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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