ライフサイエンスコーパス: osteoblastic

1 e-derived osteosarcomas were among the least osteoblastic.

2 mice suggest the commensal microbiota's anti-osteoblastic actions are mediated via local disruption o

3 PARgamma adipocytic and suppression of RUNX2 osteoblastic activities.

4 delivery of simvastatin hydroxyacid enhanced osteoblastic activity in vitro.

5 mice by targeting Gsk-3beta to activate the osteoblastic activity of endogenous stem cells, thus add

6 xpression in PCa cells and, hence, allow the osteoblastic activity of Wnts to be realized.

7 patocyte growth factor, and three markers of osteoblastic activity, procollagen I, osteocalcin, and a

8 alcin were used to identify osteoclastic and osteoblastic activity, respectively.

9 (BMP) and Wnts are mediators of PCa-induced osteoblastic activity, the relation between them in PCa

10 lead to an increase in both osteoclastic and osteoblastic activity.

11 f RUNX2 at serine 319 (Ser-319) promotes its osteoblastic activity.

12 bone-specific tracer whose uptake depends on osteoblastic activity.

13 nchymal stem cell pool and allocation to the osteoblastic and adipocytic cell lineages.

14 ells have the capacity to differentiate into osteoblastic and adipogenic lineages; recent research su

15 ) induced MES marker expression and aberrant osteoblastic and chondrocytic differentiation in a TEAD-

16 Hox mutant cells are defective in osteoblastic and chondrogenic differentiation in tri-lin

17 We demonstrate that zonal organization of osteoblastic and fibroblastic cellular phenotypes can be

18 Both osteoblastic and osteoblast-regulated osteoclastic diffe

19 bone demineralization secondary to increased osteoblastic and osteoclastic activity is the price paid

20 mitigation of leukemia-induced uncoupling of osteoblastic and osteoclastic cells may represent a nove

21 an initiate an immune response that disturbs osteoblastic and osteoclastic cellular homeostasis throu

22 suggested that compressive stress regulates osteoblastic and osteoclastic differentiation through os

23 rate that conditioned media from PTH-treated osteoblastic and osteocytic cells contain soluble chemot

24 d alpha-2-macroglobulin are highly active in osteoblastic, androgen-independent prostate cancer in vi

25 This discordance argues that osteoblastic assessment provides an incomplete assessmen

26 bone mass was neither due to the changes in osteoblastic bone formation activity nor osteoclastic bo

27 In conclusion, mBMPR1A-mFc stimulates osteoblastic bone formation and decreases bone resorptio

28 ssion in mesenchymal cells directly controls osteoblastic bone formation and indirectly regulates ost

29 Bone remodeling is a continuous process of osteoblastic bone formation and osteoclastic bone resorp

30 PTH therapy increased osteoblastic bone formation and suppressed osteoclasts.

31 evere osteoporosis was caused by a defect in osteoblastic bone formation arising from an inhibitory e

32 rophages stimulate skeletal wound repair and osteoblastic bone formation by poorly defined mechanisms

33 tro, these cells display a minimal effect on osteoblastic bone formation in mice.

34 rin-dihydropyridine hybrids that have potent osteoblastic bone formation in vitro and that prevent ov

35 recent evidences support the hypothesis that osteoblastic bone formation is impaired, a clear pathoge

36 one mass, in part, attributable to augmented osteoblastic bone formation.

37 coupling of osteoclastic bone resorption and osteoblastic bone formation.

38 n signaling, a critical anabolic pathway for osteoblastic bone formation.

39 rm sclerotic lesions that closely mirror the osteoblastic bone lesions induced by metastatic prostate

40 Osteoblastic bone metastases are the most common metasta

41 ockade strategies are commonly used to treat osteoblastic bone metastases.

42 SB conversion is one mechanism that leads to osteoblastic bone metastasis of PCa.

43 rostate cancer bone metastases are primarily osteoblastic, but the source of bone-forming cells in th

44 steoclastic reaction is required even in the osteoblastic cancer cells and the activation of NF-kappa

45 Pre-osteoblastic cell adhesion and proliferation assays reve

46 wever, the functional significance of MN1 in osteoblastic cell biology is largely unknown.

47 ormancy when they are co-cultured with a pre-osteoblastic cell line, MC3T3-E1.

48 ed a short hairpin RNA technology in a mouse osteoblastic cell line, MC3T3-E1; generated single cell-

49 presses MMP-13 gene transcription in the rat osteoblastic cell line, UMR 106-01.

50 orylation of HDAC4 in the nucleus of the rat osteoblastic cell line, UMR 106-01.

51 Pb decreased osteoblastic cell number leading to a depression of bone

52 suggest that ASPP 049 from C. comosa induced osteoblastic cell proliferation and differentiation thro

53 Wnt signaling pathways mediate SrRan-induced osteoblastic cell replication and differentiation, which

54 n our study, SPI-fed rat serum inhibited the osteoblastic cell senescence pathway.

55 -regulates caveolin-1 expression to suppress osteoblastic cell senescence pathways.

56 bone loss, in part, is a result of increased osteoblastic cell senescence, and that ST-SPI diet early

57 bone loss, in part, is a result of increased osteoblastic cell senescence, and that ST-SPI diet early

58 uced bone loss was associated with increased osteoblastic cell senescence.

59 Here, we show that alteration of the BMM by osteoblastic cell-specific activation of the parathyroid

60 ransgenic mice expressing a miR-433 decoy in osteoblastic cells (Col3.6 promoter), the amplitude of P

61 ease of adenosine-5'-triphosphate (ATP) from osteoblastic cells (MC3T3-E1) was measured in real time.

62 MC3T3-E1 osteoblastic cells and bone marrow cells were used to ve

63 n these processes in mouse long bone-derived osteoblastic cells and human Saos-2 cells.

64 The consequences of p53 loss for osteoblastic cells and OS development are poorly underst

65 and other related key signaling mediators in osteoblastic cells and osteocytes in vitro.

66 ndicate that the differentiated phenotype of osteoblastic cells and possibly osteocytes depends upon

67 s a novel target of 1,25(OH)(2)D(3) in MG-63 osteoblastic cells and that it is a coactivator for VDR-

68 d to primary cultures of mouse tibia-derived osteoblastic cells and the osteoblast UMR106 cell line a

69 genetic pulse-chase experiments that define osteoblastic cells as short-lived and nonreplicative, re

70 wever, showed p-c-Myc expression specific to osteoblastic cells at the tumor-bone interface.

71 racellular domain (NICD), and in Rosa(Notch) osteoblastic cells by Cre recombinase-mediated excision

72 NFATc1 was induced in Rosa(Notch) osteoblastic cells by transducing an adenoviral vector e

73 FATc1 on the differentiation and function of osteoblastic cells demonstrated that NICD and NFATc1 inh

74 Primary cultures for osteoblastic cells derived from Osx::CXCR4(fl/fl) mice a

75 Additionally, although osteoblastic cells derived from WT proliferate following

76 ing the cell adhesion molecule N-cadherin in osteoblastic cells forming the hematopoietic stem cell (

77 Normal osteoblastic cells have been shown to support hematopoie

78 LH2 depletion in MC3T3 osteoblastic cells impaired the formation of HLCCs, resu

79 thyroid hormone (PTH) responsiveness gene in osteoblastic cells in bone, and was investigated as a po

80 e (Dex) and TNFalpha had a similar effect on osteoblastic cells in vitro.

81 L-33 and ST2 in alveolar bone in vivo and in osteoblastic cells in vitro.

82 1-activated SREBP-1a and CREB-H in UMR106-01 osteoblastic cells increased the number of mineralized f

83 The addition of 4-HNE to cultured osteoblastic cells increases oxidative stress, which in

84 transgenic expression of active TGF-beta1 in osteoblastic cells induced osteoarthritis, whereas inhib

85 found phosphorylated/activated in endosteal osteoblastic cells located at the hedge of the hematoma.

86 e signaling by SPI-associated isoflavones in osteoblastic cells may explain the persistent effects of

87 enescence when they were introduced into pre-osteoblastic cells MC3T3-E1.

88 d osteonectin in both femurs and bone marrow osteoblastic cells of mice.

89 sfecting miR-exon4 inhibitor to the MC3T3-E1 osteoblastic cells resulted in a significant downregulat

90 t of the IGF-1 receptor (Igf1r) in their pre-osteoblastic cells showed lower bone mass and mineral de

91 onmental HSC support, and the spindle-shaped osteoblastic cells that increased with PTH treatment wer

92 Thus, in osteoblastic cells the acute proliferative effects of bo

93 hormone-related protein (PTHrP) treatment of osteoblastic cells up-regulated CCL2 and was blocked by

94 d osteogenic differentiation of MC3T3-E1 pre-osteoblastic cells were assessed.

95 Rat bone-marrow-derived osteoblastic cells were cultured on titanium disks with

96 pace, resulting in a complete loss of mature osteoblastic cells while perivascular cells are maintain

97 Treatment of UMR-106 osteoblastic cells with cKL + FGF23 increased the phosph

98 PTH or PGE2 elevated expression of MMP-13 in osteoblastic cells without affecting basal levels of the

99 activity (ie, endothelial, mesenchymal, and osteoblastic cells).

100 marrow cells and p47(phox)-Nox2 signaling in osteoblastic cells, 2-year-old p47(phox-/-) mice showed

101 e injured site, reduced number of Osterix(+) osteoblastic cells, and reduced expression of the osteob

102 In MG63 osteoblastic cells, increased expression of the 1,25(OH)

103 Within osteoblastic cells, PKCalpha enhances proliferation and

104 t, T(3) treatment inhibited Wnt signaling in osteoblastic cells, suggesting that T(3) inhibits the Wn

105 To define the effects of leukemia on osteoblastic cells, we used an immunocompetent murine mo

106 de endosteal endothelium, stromal cells, and osteoblastic cells, whereas central marrow remains vascu

107 H increases the release of amphiregulin from osteoblastic cells, which acts on the EGFRs expressed on

108 sitive control, PP was expressed in MC3T3-E1 osteoblastic cells, which normally mineralize their matr

109 Leukemic mice had inhibition of osteoblastic cells, with decreased serum levels of the b

110 rat liver, lung, brain, kidney, testis, and osteoblastic cells.

111 it PTH- or PGE2-induced MMP-13 expression in osteoblastic cells.

112 one-resident osteocalcin-expressing (Ocn(+)) osteoblastic cells.

113 a leukemia-derived secreted factor inhibited osteoblastic cells.

114 pro-apoptotic effects of Dex and TNFalpha on osteoblastic cells.

115 mulate gene transcription in mesenchymal and osteoblastic cells.

116 a more stem-like state upstream of cancerous osteoblastic cells.

117 talloproteinase-13 (MMP-13) transcription in osteoblastic cells.

118 ch and NFAT signaling pathways interacted in osteoblastic cells.

119 that are mitotically transmitted by Runx2 in osteoblastic cells.

120 uced radiation-induced apoptosis in cultured osteoblastic cells.

121 amatically during differentiation of primary osteoblastic cells.

122 ized lipids and 4-HNE stimulate apoptosis of osteoblastic cells.

123 t effects due to the additional targeting of osteoblastic cells.

124 or activation of the PTH receptor (PTH1R) in osteoblastic cells; however, the osteoblastic subset med

125 experiments revealed that OP9 cells acquired osteoblastic characteristics while down-regulating some

126 teogenesis versus adipogenesis, which favors osteoblastic commitment under binary in vitro differenti

127 expressed in the LepR(+) population without osteoblastic commitment, and the LepR(+)Runx2-GFP(low) s

128 ) is known to contribute to formation of the osteoblastic component of PCa skeletal bone metastases.

129 is an active atherosclerotic process with an osteoblastic component resembling coronary calcification

130 concentrations of 25-hydroxyvitamin D, local osteoblastic conversion of 25-hydroxyvitamin D to 1,25-d

131 of key genes required for mineralization of osteoblastic cultures in vitro and bone formation in viv

132 Mineralization in UMR 106-01 osteoblastic cultures occurs within extracellular biomin

133 romised bone repair in adult mice because of osteoblastic defects and not increased osteoclastic reso

134 in serum FGF23 levels occurred in mice with osteoblastic deletion of Cyp27b1 (12-fold) compared with

135 Conditional osteoblastic deletion of Cyp27b1 caused lower serum FGF2

136 equired for establishing HSC niches and that osteoblastic development is induced by OCLs.

137 SMCs cultured in CN serum showed accelerated osteoblastic differentiation (alkaline phosphatase activ

138 is from arachidonic acid and is critical for osteoblastic differentiation and immune behavior.

139 , we showed that aortic medial cells undergo osteoblastic differentiation and matrix calcification bo

140 hibition with OPG had little or no effect on osteoblastic differentiation and matrix calcification of

141 lx2 and Dlx6 have the potential to stimulate osteoblastic differentiation and may compensate for the

142 ion of H19 expression in LFS OBs facilitated osteoblastic differentiation and repressed tumorigenic p

143 e find that ENPP1 expression is critical for osteoblastic differentiation and that this effect is not

144 is study addressed the role of impairment of osteoblastic differentiation as a mechanism underlying p

145 ecapitulated OS features including defective osteoblastic differentiation as well as tumorigenic abil

146 an expansion of phenotypic MSPCs primed for osteoblastic differentiation at the expense of HSC-maint

147 viability of osteosarcoma cells and inhibits osteoblastic differentiation both in vitro and in vivo.

148 fracture repair phenotype and the diminished osteoblastic differentiation capacity of old animals.

149 ormulations exerted a comparable stimulus on osteoblastic differentiation even at low doses (2.5%), i

150 se in stress above 2 g/cm(2) did not enhance osteoblastic differentiation further but significantly i

151 ne morphogenetic proteins (BMPs) that induce osteoblastic differentiation have been successfully used

152 absence of Dlx5 to produce relatively normal osteoblastic differentiation in Dlx5 knockout mice, whil

153 varial mesenchyme, which results in aberrant osteoblastic differentiation in Gli3-deficient mouse (Gl

154 rinB2-Fc significantly promoted EPO-mediated osteoblastic differentiation in ST2 cells.

155 uction of this exon-exclusion event retarded osteoblastic differentiation in vitro and inhibited bone

156 Analysis of the data suggests that osteoblastic differentiation is promoted by mechanical s

157 d to examine messenger RNA expression of PDL osteoblastic differentiation markers: type I collagen, a

158 of zeste homolog 2) is down-regulated during osteoblastic differentiation of AMSCs.

159 that expression of Cdo1 was elevated during osteoblastic differentiation of BMSCs in vitro.

160 3 cells and caused more severe impairment of osteoblastic differentiation of MC3T3-E1 cells than the

161 he display of RGD and PHSRN could induce the osteoblastic differentiation of mesenchymal stem cells (

162 one matrix during bone remodeling stimulates osteoblastic differentiation of recruited mesenchymal st

163 bits proliferation and induces expression of osteoblastic differentiation regulators.

164 ation, but its effects on PDL with regard to osteoblastic differentiation remain inconclusive.

165 beta-catenin in NF1 causes a shift away from osteoblastic differentiation resulting in a pseudarthros

166 ted from Enpp1 knock-out mice show defective osteoblastic differentiation upon stimulation with ascor

167 to a fibronectin-coated surface in terms of osteoblastic differentiation using bone morphogenetic pr

168 asma (PRP) and platelet-poor plasma (PPP) on osteoblastic differentiation using primary cultures of h

169 ng adipogenesis via the former and promoting osteoblastic differentiation via NFATc1/COX2.

170 We found that EPO slightly promotes osteoblastic differentiation with the increased expressi

171 stem cells stabilized ID proteins, inhibited osteoblastic differentiation, and enhanced proliferation

172 patterns of transcription factor expression, osteoblastic differentiation, and mineralized matrix dep

173 These genes, and others triggering osteoblastic differentiation, are selectively downregula

174 tch inhibits endochondral bone formation and osteoblastic differentiation, causing severe osteopenia.

175 t Bzb induces MSCs to preferentially undergo osteoblastic differentiation, in part by modulation of t

176 one marrow nestin(+) cells and favours their osteoblastic differentiation, in vivo nestin(+) cell dep

177 rtion of mesenchymal progenitors but reduced osteoblastic differentiation, leading to impaired HSC ho

178 rease in cancellous bone volume and enhanced osteoblastic differentiation.

179 th lower expression of several inhibitors of osteoblastic differentiation.

180 ixed bone lesions, especially in controlling osteoblastic effect within tumor-harboring bone environm

181 bone lesions, comprising both osteolytic and osteoblastic elements.

182 atherosclerotic human aortas, activation of osteoblastic events, including increased expression of b

183 Further, osteoblastic expansion is not sufficient to increase HSC

184 ng in stem cells as a result of Wif1-induced osteoblastic expression of Sonic Hedgehog.

185 t this function of ATF4 occurred through its osteoblastic expression.

186 e enhanced in the presence of osteolytic and osteoblastic factors such as RANKL (receptor activator o

187 okine CCL-3 was recently reported to inhibit osteoblastic function in myeloma, we tested its expressi

188 examine whether P. gingivalis lipids inhibit osteoblastic function.

189 The osteoblastic functions of alkaline phosphatase activity

190 l lethality confound ascertaining the direct osteoblastic functions of PKD1 in adult bone.

191 Herein, we examined the role of osteoblastic GC signaling in collagen antibody-induced a

192 ficantly mitigated in animals with disrupted osteoblastic GC signaling.

193 otective dosages, the VDR activators reduced osteoblastic gene expression in the aorta, which is norm

194 Osteoblastic gene expression levels confirmed a defect o

195 nces Wnt activity and abnormal expression of osteoblastic genes (osteomimicry) that contribute to hom

196 The odds ratio of positive osteoblastic growth after a 30-second 2.5% NaOCl exposur

197 Light microscopy showed on average 97% osteoblastic growth for bone particles exposed to PovI 5

198 Best osteoblastic growth occurred after bone PovI exposure an

199 After 60-second explant exposure, positive osteoblastic growth was 7.7 times more likely to occur w

200 ring Saos2 and HOS OS cells and noncancerous osteoblastic hFOB cells.

201 orted a profound remodeling of the endosteal osteoblastic HSC niche after total body irradiation (TBI

202 single novel cytokine that could induce both osteoblastic IL-6 production and functional osteoclast f

203 bone-forming lesions, but the source of the osteoblastic lesions remains unclear.

204 e terminally differentiated cell type of the osteoblastic lineage and have important functions in ske

205 Multipotent stromal cells (MSCs) and their osteoblastic lineage cell (OBC) derivatives are part of

206 little is known about the specific roles of osteoblastic lineage cells (OBCs) in maintaining hematop

207 n this process because deletion of Vegfr2 in osteoblastic lineage cells enhanced osteoblastic maturat

208 GF2) high molecular weight (HMW) isoforms in osteoblastic lineage cells in mice resulted in phenotypi

209 WNT signaling between the hematopoietic and osteoblastic lineage cells in these diseases.

210 l (HSC) niche, resulting in the expansion of osteoblastic lineage cells that preferentially support m

211 ion, a characteristic phenotypic property of osteoblastic lineage cells, was blocked by 4-(2-aminoeth

212 nuclear factor kappaB ligand (RANKL) in the osteoblastic lineage cells, which then cause the hematop

213 These data indicate that the osteoblastic lineage is under continuous stimulation; ho

214 th haploinsufficiency of the Rb1 gene in the osteoblastic lineage reiterate the radiation susceptibil

215 early differentiation, and commitment to the osteoblastic lineage through the selective MAPKs and Sma

216 t CD34(+) cells could be differentiated into osteoblastic lineage, in vitro.

217 progenitor cells to differentiate along the osteoblastic lineage, inappropriately elevated levels of

218 a reduced ability to differentiate into the osteoblastic lineage, which was partially rescued by exo

219 -cadherin, has been targeted to cells of the osteoblastic lineage.

220 mmitment of bone marrow stromal cells to the osteoblastic lineage.

221 dant reticular (CAR) cells, and cells of the osteoblastic lineage.

222 nificantly higher uptake than the moderately osteoblastic LM8 (P < 0.05) and the osteolytic 143B (P <

223 these results identify a mechanism by which osteoblastic Lrp4 controls osteoclastogenesis, reveal a

224 or sclerostin was unaltered, indicating that osteoblastic Lrp4 retains sclerostin within bone.

225 stological staining as well as expression of osteoblastic marker (OPN, Runx2 and OSX).

226 Also, suppressed osteoblastic marker expression in NZO cells may contribu

227 manipulation also restores the expression of osteoblastic marker genes, namely Ocn and bone sialoprot

228 lls have been identified by staining for the osteoblastic marker, osteocalcin (OCN).

229 matrix mineralization and the expression of osteoblastic markers (Runx2,Col1a1,Bglap2,Sp7,Atf4, andA

230 CRB-15 prevented the suppression of osteoblastic markers of bone formation, and reduced oste

231 rtance of coupling matrix remodeling through osteoblastic matrix deposition and osteoclastic tissue r

232 egfr2 in osteoblastic lineage cells enhanced osteoblastic maturation and mineralization.

233 Osteoblastic maturation is restored in TRE17-expressing

234 ids have the opposite effect, ie, inhibiting osteoblastic maturation.

235 formation capture analysis in the murine pre-osteoblastic MC3T3-E1 cell line revealed increased conta

236 e analysis of the RUNX2 cistrome in both pre-osteoblastic MC3T3-E1 cells (POB) and their mature osteo

237 id A (A-SAA/Saa3) was shown before to affect osteoblastic metabolism.

238 ling has been shown to promote the growth of osteoblastic metastases and to potentiate signaling via

239 gher in preosteoblastic MC3T3-E1 cells, late osteoblastic MLO-A5 cells, and MLO-Y4 osteocytes, consis

240 The effect of CTGF and EMD on osteoblastic mRNA expression in PDL cells is not obvious

241 Lack of osteoblastic N-cadherin did not block the bone anabolic

242 This report demonstrates that osteoblastic N-cadherin is not required for regulation o

243 To determine whether osteoblastic N-cadherin is required for HSC regulation,

244 g for Wnt activity that could contribute the osteoblastic nature of PCa.

245 ory evidence of the roles of vascular versus osteoblastic niche components in HSPC function.

246 tate cancer cells preferentially home to the osteoblastic niche in the bone marrow, where they compet

247 megakaryocytes (MKs) from the proliferative osteoblastic niche to the capillary-rich vascular niche

248 PKH(+) MM cells prefer to reside within the osteoblastic niches of the bone marrow (PKH(+)/OS) rathe

249 Our data indicate that osteoblastic niches support the growth of quiescent PKH(

250 Activation of PTH1R in osteocytes increases osteoblastic number and bone mass.

251 h pre-osteoblastic (POBs) and differentiated osteoblastic (OBs) MC3T3-E1 cells, and assessed localiza

252 ne marrow from rat MB and LB was cultured in osteoblastic or osteoclastic differentiation media.

253 both endothelial progenitor (CD34, KDR) and osteoblastic (osteocalcin [OCN]) cell surface markers.

254 vation drove bone accumulation by modulating osteoblastic/osteoclastic cross-talk through the direct

255 in the bone, both in the osteolytic PC3 and osteoblastic/osteoclastic mixed C4-2B cells; while the a

256 LNCaP cells resulted in the formation of an osteoblastic/osteoclastic mixed tumor with increased ost

257 expression of MMP-13 in UMR 106-01 cells, an osteoblastic osteosarcoma cell line.

258 ese studies demonstrate a molecular role for osteoblastic PHD/VHL/HIF signaling that can be targeted

259 irculating endothelial progenitor cells with osteoblastic phenotype (EPC-OCN) in human aortic valve c

260 rker of bone remodeling, correlated with the osteoblastic phenotype.

261 rophy, but also subsequent acquisition of an osteoblastic phenotype.

262 n through EphB4 shRNA inhibited EPO-mediated osteoblastic phenotypes.

263 ,25(OH)2D3 on the transcriptomes of both pre-osteoblastic (POBs) and differentiated osteoblastic (OBs

264 ate Wnt signaling in osteoblasts; expand the osteoblastic pool; and increase bone turnover, bone mine

265 l cells and in dysfunctional mesenchymal and osteoblastic populations, whereas megakaryocytes were de

266 nduced by phenamil selectively in cells with osteoblastic potential.

267 yperglycemia in bone marrow diverts dividing osteoblastic precursor cells (bone marrow stromal cells)

268 VEGF is highly expressed in osteoblastic precursor cells and is known to stimulate b

269 Mice with conditional VEGF deficiency in osteoblastic precursor cells exhibited an osteoporosis-l

270 ENPP1 is also expressed in osteoblastic precursor cells when stimulated with FGF2,

271 se in bone mineralization and sclerosis, the osteoblastic process can also be detected morphologicall

272 ls, characterized by potent induction of the osteoblastic production of interleukin-6 (IL-6), an infl

273 tration, compound 11 significantly inhibited osteoblastic proteosomal activity.

274 inhibited by dBSP via down-regulation of the osteoblastic RANKL production.

275 poptosis but did not prevent the increase in osteoblastic RANKL.

276 ribute the phenotype of OTR deficiency to an osteoblastic rather than an osteoclastic defect.

277 ate cancer xenografts whose cells induced an osteoblastic reaction in bone and in the subcutis of imm

278 is androgen-independent and induces a robust osteoblastic reaction in bonelike matrix and soft tissue

279 ysical properties and adversely affected the osteoblastic response irrespective of their observed ant

280 tion of specific PHD isoforms fine-tunes the osteoblastic response to hypoxia, thereby directing two

281 cells (LNCaP-PDGF-D) revealed osteolytic and osteoblastic responses similar to those observed in huma

282 iability of human mesenchymal stem cells and osteoblastic SaOS-2 cells was increased on all ND surfac

283 In the osteoblastic Saos2 cell line, ANGPTL4 caused a dose-depe

284 ematopoietic stem cells (HSCs) interact with osteoblastic, stromal, and vascular components of the BM

285 (PTH1R) in osteoblastic cells; however, the osteoblastic subset mediating this action of PTH is unkn

286 apeutic response likely arises from enhanced osteoblastic support and the stimulation of VEGF by ACTH

287 lag time, as well as higher osteoid surface, osteoblastic surface, resorption surface, and osteoclast

288 and retinoid X receptor to the promoters of osteoblastic target genes.

289 introduced into the model grow and colonize osteoblastic tissue in a manner reflecting various chara

290 of Dkk1 suppressed aortic expression of the osteoblastic transcription factor Runx2, increased expre

291 s is associated with decreased expression of osteoblastic transcription factors and inhibition of c-J

292 f nuclear factor-kappaB ligand and increased osteoblastic tumor necrosis factor superfamily member 11

293 an embryonic kidney HEK-TSHR cells and human osteoblastic U2OS-TSHR cells.

294 ession is highly induced by PTH treatment in osteoblastic UMR 106-01 cells, as well as primary osteob

295 cked by the SIRT1 activator, resveratrol, in osteoblastic UMR 106-01 cells.

296 Mechanistically, osteoblastic VDR signaling suppressed calcium incorporat

297 a differential role of GTPases in endosteal/osteoblastic versus perivascular niche function.

298 iated cytotoxicity of the bone substitute to osteoblastic viability and function, implying enhanced b

299 Here we report that osteoblastic Wif1 overexpression disrupts stem cell quie

300 ied mouse models with either constantly high osteoblastic Wnt16 expression or no Wnt16 expression.