ライフサイエンスコーパス: osteoblastic

1 e-derived osteosarcomas were among the least osteoblastic.

2 s A total of 64 metastases (38 predominantly osteoblastic, 26 predominantly osteolytic) were detected

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

4 PARgamma adipocytic and suppression of RUNX2 osteoblastic activities.

5 tic and collagenase activity and increase in osteoblastic activity are possibly involved in this proc

6 teoclastic bone resorption without affecting osteoblastic activity in bone.

7 tween, and determinants of, osteoclastic and osteoblastic activity in stunted infants/children, and s

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

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

10 tic activity without affecting biomarkers of osteoblastic activity or improving their severe stunting

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

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

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

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

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

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

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

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

19 Both osteoblastic and osteoblast-regulated osteoclastic diffe

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

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

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 sequences for the detection of predominantly osteoblastic and osteolytic metastases were determined b

25 liable differentiation between predominantly osteoblastic and osteolytic spine metastases with a high

26 MRI for the differentiation of predominantly osteoblastic and osteolytic spine metastases.

27 udy aims to unveil the role of Histatin-1 in osteoblastic and vascular cell lineages challenged with

28 n beta-catenin protein, colony forming units osteoblastic, and the amount of bone at the fracture sit

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

30 This discordance argues that osteoblastic assessment provides an incomplete assessmen

31 nical integrity, working characteristics and osteoblastic biocompatibility of bone cement.

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

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

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

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

36 PTH therapy increased osteoblastic bone formation and suppressed osteoclasts.

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

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

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

40 Both drugs were found to enhance osteoblastic bone formation in vivo using a unique gene

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

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

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

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

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

46 Clinical osteoblastic bone metastasis samples had higher levels o

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

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

49 Pre-osteoblastic cell adhesion and proliferation assays reve

50 may be associated with decreasing fetal pre-osteoblastic cell differentiation, under epigenetic cont

51 In vitro experiments using an osteoblastic cell line highlight that cosurface stimulat

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

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

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

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

56 assessed using NIH/3T3 fibroblasts and MG-63 osteoblastic cell lines, respectively.

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

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

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

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

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

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

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

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

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

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

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

68 we found prostaglandin E2 (PGE2) secreted by osteoblastic cells activates PGE2 receptor 4 (EP4) in se

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

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

71 firmed the NACA-PP1A interaction in MC3T3-E1 osteoblastic cells and observed that NACA phosphorylatio

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

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

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

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

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

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

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

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

80 Additionally, although osteoblastic cells derived from WT proliferate following

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

82 The transdifferentiation of malignant osteoblastic cells from malignant chondroblastic cells i

83 Normal osteoblastic cells have been shown to support hematopoie

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

85 We have cultured MC3T3-E1 mouse osteoblastic cells in biomimetic microcracked hydroxyapa

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

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

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

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

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

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

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

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

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

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

96 ory nerves or cyclooxygenase-2 (COX2) in the osteoblastic cells significantly reduces bone volume in

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

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

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

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

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

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

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

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

105 kappa B ligand (RANKL), increased osterix(+) osteoblastic cells, and decreased smoothness of the cort

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

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

108 Within osteoblastic cells, PKCalpha enhances proliferation and

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

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

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

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

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

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

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

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

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

118 a leukemia-derived secreted factor inhibited osteoblastic cells.

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

120 mulate gene transcription in mesenchymal and osteoblastic cells.

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

122 ch and NFAT signaling pathways interacted in osteoblastic cells.

123 ese genes were switched on by coculture with osteoblastic cells.

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

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

126 uced radiation-induced apoptosis in cultured osteoblastic cells.

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

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

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

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

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

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

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

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

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

136 Conditional osteoblastic deletion of Cyp27b1 caused lower serum FGF2

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

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

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

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

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

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

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

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

154 During osteoblastic differentiation in vitro, CD200(+) cells ex

155 late hMSC adhesion, paracrine signaling, and osteoblastic differentiation in vitro.

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

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

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

159 3 cells and caused more severe impairment of osteoblastic differentiation of MC3T3-E1 cells than the

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

161 osteogenesis by driving the recruitment and osteoblastic differentiation of mesenchymal stromal cell

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

163 erythrocyte extravasation and lysis promotes osteoblastic differentiation of smooth muscle cells and

164 bits proliferation and induces expression of osteoblastic differentiation regulators.

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

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

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

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

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

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

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

174 the control of OPN and OCN expression during osteoblastic differentiation.

175 ne expression profiles associated with early osteoblastic differentiation.

176 tion factor 2, a nuclear protein involved in osteoblastic differentiation.

177 th lower expression of several inhibitors of osteoblastic differentiation.

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

179 bone lesions, comprising both osteolytic and osteoblastic elements.

180 Further, osteoblastic expansion is not sufficient to increase HSC

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

182 Nuclear localization of the pro-osteoblastic factor RUNX2 on soft and stiff substrates s

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

184 in level, and increased colony forming units osteoblastic from bone marrow cells.

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

186 examine whether P. gingivalis lipids inhibit osteoblastic function.

187 The osteoblastic functions of alkaline phosphatase activity

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

189 ficantly mitigated in animals with disrupted osteoblastic GC signaling.

190 Osteoblastic gene expression levels confirmed a defect o

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

192 Though expression of osteoblastic genes was increased, the levels of osteocla

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

194 Best osteoblastic growth occurred after bone PovI exposure an

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

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

197 mib markedly increased protein levels of the osteoblastic key transcription factor osterix/Sp7 (Osx).

198 e cancer bone metastases that contributes to osteoblastic lesion formation by blocking osteoclast dif

199 Prostate cancer cell lines that induce mixed osteoblastic lesions in bone expressed 5-6 times more No

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

227 Osteoblastic maturation is restored in TRE17-expressing

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

229 o induce in vitro biomineralization from pre-osteoblastic MC3T3 cells and human mesenchymal stem cell

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

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

232 Mouse osteoblastic (MC3T3-E1) and endothelial (human umbilical

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

234 cificity of 73% (19 of 26) for predominantly osteoblastic metastases and a sensitivity of 73% (19 of

235 cificity of 96% (25 of 26) for predominantly osteoblastic metastases and a sensitivity of 96% (25 of

236 porates into newly formed bone matrix within osteoblastic metastatic lesions.

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

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

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

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

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

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

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

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

245 Thus, engagement of myeloma cells with the osteoblastic niche induces expression of a suite of myel

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

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

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

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

250 Osteoblastic number was significantly lower, but osteocl

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 tic osteosarcoma lesions compared to primary osteoblastic osteosarcoma lesions.

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

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

261 The acquisition of an osteoblastic phenotype in VICs that come into contact wi

262 h RBCs resulted in a global inflammatory and osteoblastic phenotype, reflected by the up-regulation o

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

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

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

266 nhibition of MMP-3 rescued the NICD3-induced osteoblastic phenotypes.

267 ,25(OH)2D3 on the transcriptomes of both pre-osteoblastic (POBs) and differentiated osteoblastic (OBs

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

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

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

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

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

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

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

275 tration, compound 11 significantly inhibited osteoblastic proteosomal activity.

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

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

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 alize in the bone where they induce a unique osteoblastic response.

282 Secondary outcomes included osteoblastic responses as measured biochemically and rad

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

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

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

286 ytes; in contrast, transgenic mice (Tg) with osteoblastic-specific deletion of Epor exhibit reduced t

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

288 gulatory genes spanning new fibroblastic and osteoblastic subpopulations including distinct osteoblas

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

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

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

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

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

294 osteoblastogenesis, while loss of Notch3 in osteoblastic tumors enhanced osteolytic lesion area and

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

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

297 Mechanistically, osteoblastic VDR signaling suppressed calcium incorporat

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

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.