ライフサイエンスコーパス: osteoblast

1 sion of progenitors into odontoblasts versus osteoblasts.

2 from imbalanced activity of osteoclasts and osteoblasts.

3 x2 complexes is altered in Dchs1/Fat4 mutant osteoblasts.

4 the DNA damage and apoptotic rates in Fto KO osteoblasts.

5 produce signals that alter bone formation by osteoblasts.

6 nalling dysfunction occurring in primary AIS osteoblasts.

7 ositively regulates MPC differentiation into osteoblasts.

8 nsible for lifelong generation of periosteal osteoblasts.

9 lance to the others, or to primary calvarial osteoblasts.

10 ing to the differentiation of the DPSCs into osteoblasts.

11 C receptor (GR) was deleted in stromal cells/osteoblasts.

12 Homer1 associates with CaSR in primary human osteoblasts.

13 e bone and also co-localize in primary human osteoblasts.

14 TH stimulated the transfer of fatty acids to osteoblasts.

15 een A2AR, beta-catenin, and Akt signaling in osteoblasts.

16 mulation and cellular beta-catenin levels in osteoblasts.

17 oprogenitors and a corresponding increase in osteoblasts.

18 rease IL18 and IL1B gene expression in human osteoblasts.

19 last differentiation) expression in MC3T3-E1 osteoblasts.

20 TORC2 and thereby stabilizes beta-catenin in osteoblasts.

21 sporine, a chemical mediator of apoptosis in osteoblasts.

22 on of MSCs into adipocytes at the expense of osteoblasts.

23 letal progenitor stem cells and bone-forming osteoblasts.

24 less proliferative potential than Keap1(+/-) osteoblasts.

25 o-stimulant of the bone-building activity of osteoblasts.

26 of human mesenchymal stem cells (MSCs) into osteoblasts.

27 or the differentiation and mineralization of osteoblasts.

28 production of paracrine factors controlling osteoblast activity.

29 rkedly enhanced bone formation via augmented osteoblast activity.

30 he control of bone homeostasis by regulating osteoblast activity.

31 lls and Saos-2 cells as a valuable model for osteoblast adhesion.

32 tent to which PA MSCs and CD271+ MSCs formed osteoblasts, adipocytes or chondrocytes in vitro.

33 esenchymal phenotypes, such as odontoblasts, osteoblasts, adipocytes, and myoblasts.

34 rment of melatonin receptor signaling in AIS osteoblasts allowing the classification of patients into

35 bone matrix differentiates from bone-forming osteoblasts; although osteoblast differentiation require

36 The coatings did not negatively impact osteoblast and fibroblast cells growth and were capable

37 Osteoblast and inflammatory cell counts were counted on

38 is and autophagy, is known to be involved in osteoblast and myeloid differentiation, but its role in

39 ur data show that CCR3 deficiency influences osteoblast and osteoclast differentiation and that it is

40 losely associated with inflammation, affects osteoblast and osteoclast differentiation, and may play

41 orphometric analysis revealed a reduction of osteoblast and osteoclast parameters in tibiae of cystin

42 we specifically identify a dramatic loss of osteoblasts and alterations in endothelial cell function

43 rectly reduces osteoclastogenesis, increases osteoblasts and bone formation, and suppresses bone marr

44 Epor is also expressed on bone forming osteoblasts and bone loss accompanies EPO-stimulated ery

45 extensive communication between bone-forming osteoblasts and bone-resorbing osteoclasts to orchestrat

46 sms that are independent of the bone forming osteoblasts and bone-resorbing osteoclasts.

47 g cell cycle exit and the differentiation of osteoblasts and chondrocytes during skeletal development

48 one marrow mesenchymal stem cells (BMSCs) to osteoblasts and chondrocytes was reduced, and migration

49 apidly migrate toward an injury site, supply osteoblasts and chondrocytes, and recover new periosteum

50 ed by exercise, stimulates bone formation by osteoblasts and increases bone strength, but the mechani

51 modeling and conversion of chondrocytes into osteoblasts and marrow adipocytes as conserved features

52 t in the areas of new bone formation rich in osteoblasts and newly-embedded osteocytes.

53 itochondrial respiratory chain deficiency in osteoblasts and osteoclasts in PolgA(mut/mut) mice compa

54 e, our results indicated that the numbers of osteoblasts and osteoclasts were decreased in the proxim

55 and the bone microenvironment stromal cells (osteoblasts and osteoclasts), and also the effects of FG

56 one microenvironment stromal cells including osteoblasts and osteoclasts, and effectively suppress bo

57 are abundant in bone marrow and can regulate osteoblasts and osteoclasts, we examined whether gut mic

58 ipokine secretion and the differentiation of osteoblasts and osteoclasts.

59 rize the effects of cystinosin deficiency on osteoblasts and osteoclasts.

60 o cell death in nearby exposed tumour cells, osteoblasts and osteoclasts.

61 xperiments showed an impairment of Ctns(-/-) osteoblasts and osteoclasts.

62 nes, and exists in many cell types including osteoblasts and osteoclasts.

63 osteoclastogenic protein RANKL) in cultured osteoblasts and osteocytes from Notch2(tm1.1Ecan) mice.

64 direct differentiation of chondrocytes into osteoblasts and osteocytes in the TMJ.

65 Conditional deletion of Piezo1 in osteoblasts and osteocytes notably reduced bone mass and

66 osteoblastogenesis and promote apoptosis of osteoblasts and osteocytes, resulting in decreased bone

67 skeletal remodeling in part by its action on osteoblasts and osteocytes.

68 accessibility, as well as transcriptomes, of osteoblasts and other cells in uninjured and regeneratin

69 owed a significant increase in the number of osteoblasts and reduction in osteoclast surface/bone sur

70 he ability of these probes to bind to active osteoblasts and their mineral deposits and highlight the

71 eir specific targets in vitro-differentiated osteoblasts, and not to undifferentiated MSCs, and emit

72 tion by osteoclasts followed by formation by osteoblasts, and osteoclasts are a source of bone format

73 mineral present in bone that is produced by osteoblasts, and therefore provides a functional marker

74 r cells can differentiate into adipocytes or osteoblasts, and we found that NKX1-2 both promotes ST2

75 Osteoblasts are specialized mesenchymal cells that synth

76 Osteoblasts are versatile cells involved in multiple who

77 bones, the transgene was highly expressed in osteoblasts at an early stage of differentiation.

78 r osterix-positive MSC/osteoprogenitors into osteoblasts at sites that are innately osteogenic.

79 ease in the number of active osteoclasts and osteoblasts at the tumor-bone interface, without any eff

80 1 derived cell lines are imperfect models of osteoblast biology, and reinforce the importance of clea

81 oligosaccharides (HMOs), and osteoclast and osteoblast biology, young germ-free mice were colonized

82 rivative subclones are widely used models of osteoblast biology.

83 ot faithfully replicate these key aspects of osteoblast biology.

84 as proliferation and differentiation of pre-osteoblasts, but the biological mechanisms involved in t

85 cited an antianabolic sympathetic imprint in osteoblasts, but with net bone gain.

86 Luteolin, dose-dependently increased osteoblast cell counts.

87 s dsRNA accumulation and cell death in human osteoblast cell cultures.

88 y(I:C)] or genetic (Alu) dsRNA induces human osteoblast cell death.

89 ents DICER1 dysregulation- and dsRNA-induced osteoblast cell death.

90 Osteoblast cell number was higher and osteoclast and inf

91 Like osteoblast cell numbers, BMP-2 expressions were also ele

92 mouse bone marrow vascular, perivascular and osteoblast cell populations at single-cell resolution, b

93 lating RunX2 transcriptional activity in pre-osteoblast cells in a TAZ-dependent manner.

94 trode layout on the dynamics of cultured pre-osteoblast cells.

95 s, but not in normal prostatic epithelial or osteoblast cells.

96 n MSC-like intermediate state that generated osteoblasts, chondrocytes, adipocytes, and macrophages.

97 n of Nrf2, ALP and wnt5a in cultured primary osteoblasts compared to WT control.

98 teoclasts enhanced mineralization of ex vivo osteoblast cultures, an effect that was abrogated by Cth

99 s in autogenous onlay bone grafts and in pre-osteoblasts cultures, but such procedure has never been

100 In the mouse, the osteoblast-derived hormone Lipocalin-2 (LCN2) suppresses

101 Osteocalcin (OCN) is an osteoblast-derived hormone with pleiotropic physiologica

102 Secretory amounts and patterns of osteoblast-derived proteins such as osteopontin (OPN) an

103 tein TG-interacting factor 1 (Tgif1) impairs osteoblast differentiation and activity, leading to a re

104 Inhibition of USP7 regulates osteoblast differentiation and adipocyte differentiation

105 Si has been demonstrated to stimulate osteoblast differentiation and bone mineralisation in vi

106 uction in bone cells plays a pivotal role in osteoblast differentiation and bone remodelling.

107 -like receptor 2 (TLR2) and to inhibit mouse osteoblast differentiation and function through engageme

108 impacting cJUN transcriptional activity and osteoblast differentiation and function.

109 Conversely, osteoblast differentiation and mineralization were inhib

110 Osteoblast differentiation and mineralization were stimu

111 The metabolic requirements of osteoblast differentiation and mineralization, both esse

112 Osteoblast differentiation and proliferation are regulat

113 medium from NICD3-expressing cells enhanced osteoblast differentiation and proliferation in vitro, w

114 er activated genes included sets involved in osteoblast differentiation and response to oxidative str

115 The osteoblast differentiation capacity of skeletal stem cel

116 yse the role of Dchs1-Fat4 signalling during osteoblast differentiation in mouse.

117 t and mechanisms linking maternal obesity to osteoblast differentiation in offspring.

118 that increased glycolysis is associated with osteoblast differentiation in response to Wnt signaling,

119 erious effects on bone volume in vivo and on osteoblast differentiation in vitro.

120 eage cells, and deletion of Glut1 diminished osteoblast differentiation in vitro.

121 eration of osteoprogenitors is increased and osteoblast differentiation is delayed.

122 regulating the balance between adipocyte and osteoblast differentiation of bone marrow mesenchymal pr

123 was identified as osteoinductive, enhancing osteoblast differentiation of bone marrow stromal cells.

124 LKB1 deficiency increased proliferation and osteoblast differentiation of Ctsk+ periosteal cells, wh

125 analysis reveal differences in adipocyte and osteoblast differentiation pathways, bone marrow neoplas

126 ning how prostate metastases subvert the MSC-osteoblast differentiation program.

127 and migration, and completely blocks the MSC-osteoblast differentiation program.

128 ates from bone-forming osteoblasts; although osteoblast differentiation requires EphrinB2, osteocytes

129 g osteogenic stimulation efficiently induced osteoblast differentiation through Osx stabilization.

130 teoblastic subpopulations including distinct osteoblast differentiation trajectories.

131 la) was sufficient to inhibit Panx3-mediated osteoblast differentiation via reduction of Osterix and

132 ce osterix (transcription factor involved in osteoblast differentiation) expression in MC3T3-E1 osteo

133 e transcription factor RunX2, which controls osteoblast differentiation, is reduced in Pkd1 mutant mi

134 entify Dchs1-Fat4 as a signalling pathway in osteoblast differentiation, reveal its crucial role with

135 ivator of nuclear factor kappa-B ligand, and osteoblast differentiation-associated genes.

136 f Osx level to fine-tune its activity during osteoblast differentiation.

137 ed proliferation and concurrent induction of osteoblast differentiation.

138 that Dchs1-Fat4 signalling is essential for osteoblast differentiation.

139 of the serine 68 residue (Ser68) to promote osteoblast differentiation.

140 distinct requirements for Yap and Taz during osteoblast differentiation.

141 a critical transcription factor required for osteoblast differentiation.

142 nt manner, without affecting TNF activity or osteoblast differentiation.

143 cells at different stages of odontoblast and osteoblast differentiation.

144 providing both more cells and more fuel for osteoblasts during bone formation.

145 in human mesenchymal progenitor cell-derived osteoblasts employing a massively parallel, high resolut

146 steoblast via PCa-EVs and show the effect on osteoblast endogenous transcript abundance.

147 mutations stimulated the TGF-beta pathway in osteoblasts, enhanced nuclear translocation and target g

148 s why mice lacking the IL-6 receptor only in osteoblasts exhibit a deficit in exercise capacity of si

149 Normal osteoblasts express estrogen receptor alpha (ERalpha); h

150 by MM cells, yet bone stromal cells such as osteoblasts expressed and upregulated NGF when cultured

151 With loss of Hox11 function, however, osteoblasts fail to mature, with no progression to osteo

152 nverse relationship between adipocyte versus osteoblast fate selection from stem cells is implicated

153 al stromal cells (MSCs)/osteoprogenitors and osteoblasts following the injection of ZOL, in vivo.

154 loading is a critical source of bone forming osteoblasts for maximal lamellar formation and is essent

155 adation of TRAF3 in murine MPCs and inhibits osteoblast formation through GSK-3beta-mediated degradat

156 ta-catenin degradation in MPCs and maintains osteoblast formation.

157 impaired differentiation of EOCCs to mature osteoblasts from HFD obese dams.

158 Primary osteoblasts from low protein diet fed mice showed decrea

159 g Fto globally (Fto (KO) ) or selectively in osteoblasts (Fto (Oc) (KO) ).

160 one mass in SCD mice mainly through enhanced osteoblast function and increased osteoblast-related gen

161 Impairment of osteoblast function and osteoporosis has been described

162 o increased inflammatory cytokines, impaired osteoblast function, and bone loss in SCD mice.

163 in increased osteoclast activity, decreased osteoblast function, and immunosuppressed marrow microen

164 te physiology is distinct from the effect on osteoblast function.

165 opontin (OPN) and osteocalcin (OCN) modulate osteoblast function.

166 ated by increased sclerostin, which suppress osteoblast functions and promote browning of white adipo

167 ntrol of osteogenesis, and markedly prevents osteoblast generation and mineralization.

168 While the effect of Brucella infection on osteoblasts has been extensively evaluated, little is kn

169 steopenia in Keap1(-/-) mice, and Keap1(-/-) osteoblasts have significantly less proliferative potent

170 port this model, we altered the structure of osteoblast HS genetically to make it incapable of bindin

171 resulted in an altered energy homeostasis of osteoblasts, impaired mineralization and reduced bone ma

172 y are expected to preserve bone formation by osteoblasts in contrast to current treatments.

173 s present at high levels in chondrocytes and osteoblasts in mouse growth plates.

174 t cancer cells-activated FGFR siganalling in osteoblasts, including increased expression of RANKL, M-

175 PGE2 secreted by osteoblasts increases when bone density decreases as dem

176 expression of Lrp4 by both the adipocyte and osteoblast is required for normal sclerostin endocrine f

177 conclusion, endogenous EPO-Epor signaling in osteoblasts is important in bone remodeling, particularl

178 development, but its mechanism of action in osteoblasts is not well-characterized.

179 cular bone and endogenous Epor expression in osteoblasts is required for bone loss accompanying EPO-s

180 a cells and cells of the bone stroma such as osteoblasts, is yet to be fully explored.

181 In addition, primary mouse calvarial osteoblasts isolated from CCR3-deficient mice showed inc

182 antimigratory effects of zoledronic acid in osteoblast-like and endothelial cells.

183 signals colocalized with calcified areas or osteoblast-like cells in human vascular lesions.

184 steogenesis, as evidenced by increased human osteoblast-like MG-63 cell proliferation in vitro and ca

185 eaks (DSBs), in human cervix cancer HeLa and osteoblast-like MG-63 cells.

186 lized 3.6Col1a1-tk mice in which replicating osteoblast lineage cells can be ablated in an inducible

187 Our objective was to ablate proliferating osteoblast lineage cells in order to investigate the imp

188 (rAAV9) is highly effective for transducing osteoblast lineage cells in the bone.

189 1 is a mechanosensitive ion channel by which osteoblast lineage cells sense and respond to changes in

190 Osteoclasts act upon osteoblast lineage cells throughout their differentiatio

191 lucose consumption in the primary culture of osteoblast lineage cells, and deletion of Glut1 diminish

192 Additional interactions of osteoclasts with osteoblast lineage cells, including interactions with ca

193 rt through stimulating glucose metabolism in osteoblast lineage cells.

194 Differentiation in the osteoblast lineage initiates with Runx2 expression, whic

195 family member 7B (Wnt7b) transiently in the osteoblast lineage of postnatal mice, with or without co

196 S immobilizes secreted OPG at the surface of osteoblasts lineage cells, which facilitates binding of

197 mRNA expression of osteoblast markers such as Osx, Ocn and Col1a1 was unaff

198 ct on bone formation with elevated levels of osteoblast markers.

199 es marked by sox10 and col2a1a contribute to osteoblasts, marrow adipocytes, and mesenchymal cells wi

200 plex and co-regulator alpha (NACA) regulates osteoblast maturation and activity.

201 Following mechanical loading, osteoblasts may arise via activation, differentiation, o

202 malian vertebrates, the dedifferentiation of osteoblasts may contribute to skeletal regeneration.

203 evance of cellular metabolic rewiring during osteoblast-mediated bone formation and bone-turnover.

204 gment of Parathyroid hormone (PTH) activates osteoblast-mediated bone formation and is used in patien

205 meostasis is maintained by a balance between osteoblast-mediated bone formation and osteoclast-driven

206 However, it does not have any effect on osteoblast-mediated bone formation in vitro.

207 d by osteoclast-mediated bone resorption and osteoblast-mediated bone formation, represents a highly

208 ecruitment and bone resorption, and impaired osteoblast-mediated bone formation.

209 show that PPARdelta acts as key regulator of osteoblast metabolism and highlight the relevance of cel

210 ed receptor (PPAR) delta as key regulator of osteoblast metabolism.

211 s of notochord sheath segmentation, altering osteoblast migration to the developing spine, and increa

212 ption factors c-Fos and JunB, but stimulated osteoblast mineralization by regulating bone morphogenet

213 alter mesenchymal stem cell proliferation or osteoblast mineralization in vitro, nor was there eviden

214 poptosis of endothelial cells (HUVEC) and on osteoblast mineralization of vascular smooth muscle cell

215 Using osteoblast models, the identified mutations are demonstr

216 of genes that are significantly enriched in osteoblast, neuronal, and mitochondrial functions.

217 e with conditional deletion of Nf1 in mature osteoblasts (Nf1(fl/fl);Dmp1-Cre) and Mekk2(-/-) each di

218 and negatively correlated with BV/TV and the osteoblast number (both P < 0.01).

219 inhibition, or local P-SSC ablation reduces osteoblast number and delays bone healing.

220 In contrast, osteoblast number was increased 3-8-fold with PTH treatm

221 ment with E197 did not affect osteoclast and osteoblast numbers and hence did not impair bone formati

222 necessary for the ability of PTH to increase osteoblast numbers and stimulate bone formation.

223 ss of lamin A/C in skeletal muscles, but not osteoblast (OB)-lineage cells, results in not only muscl

224 f Lrp4 in the adipocyte (AdDeltaLrp4) or the osteoblast (ObDeltaLrp4).

225 high-fat diet induced greater DNA damage in osteoblast of Fto (Oc KO) mice compared to controls.

226 2 functions as a MAP3K in the ERK pathway in osteoblasts, offering a potential new therapeutic strate

227 ifferentiation of ESCs to closely associated osteoblast or chondrocyte lineages.

228 ) could influence the function of progenitor osteoblasts or adipocytes and hence determine skeletal p

229 ssociated calcifications express markers for osteoblasts, osteoclasts and osteocytes, and that bone m

230 ting independence of EPO signaling in mature osteoblasts, osteoclasts, and adipocytes.

231 There were no differences in numbers of osteoblasts, osteoclasts, and marrow adipocytes in Tg mi

232 re noted in AB volume between genotypes, but osteoblast/osteocyte markers were increased in all KOs,

233 calreticulin/calcineurin axis and increased osteoblast output from both control and calreticulin-def

234 lls when grown in co-culture with EV-treated osteoblasts (p < 0.005).

235 Because osteoclasts (OCs) and osteoblasts play a key role in bone remodeling, and MF m

236 icantly reduced bone formation rate, reduced osteoblast population densities, increased osteoclast po

237 Osteoblast precursor cell line (MC3T3-E1) and primary mu

238 iescent Cxcl12-creER(+) BMSCs transform into osteoblast precursor cells in a manner mediated by canon

239 sorption of a quantum of bone is followed by osteoblast precursor recruitment; these cells differenti

240 Here we show that upon Rankl induction, osteoblast progenitors up-regulate expression of the che

241 , in cocultures of bone marrow adipocyte and osteoblast progenitors, PTH stimulated the transfer of f

242 xpressing osteoblasts, Taz does not regulate osteoblast proliferation and Taz-Tead activity is unaffe

243 We conclude that osteoblast proliferation induced by mechanical loading i

244 enous RNA of miR-701-3p that could influence osteoblast proliferation, migration, and apoptosis in vi

245 1-3p/FGFR3 axis is an important regulator of osteoblast proliferation, migration, and apoptosis, and

246 Osteoblast proliferation, migration, and survival are pi

247 he regulatory role of lncRNA KCNQ1OT1 during osteoblast proliferation, migration, and survival.

248 o a skeletal cell type with dual chondrocyte/osteoblast properties.

249 h enhanced osteoblast function and increased osteoblast-related genes (Runx2 and Igf1) expression in

250 ver 100-fold higher-level expression of many osteoblast-related genes including osteopontin and osteo

251 The expression of osteoblast-related markers in hDFC was analysed with RT-

252 The unique function of osteoblasts requires substantial amounts of energy produ

253 T1 were prone to turning into adipocytes and osteoblasts, respectively, after differentiation inducti

254 steoclasts and stimulating bone formation by osteoblasts, respectively.

255 osteoclasts and stimulates bone formation by osteoblasts, respectively.

256 differentiation of cells to odontoblasts or osteoblasts, respectively.

257 repairable membrane injuries in bone-forming osteoblasts, resulting in release of ATP and stimulation

258 RNA-based gene-silencing assays with primary osteoblasts revealed that both CaSR and Homer1 are requi

259 ependent differentiation of odontoblasts and osteoblasts; RUNX2-S319-P was reduced in PDLs from Ddr2(

260 human kinase and phosphatase targets on pre-osteoblast SaOS-2 cells.

261 r the last 15 years, studies have shown that osteoblasts secrete endocrine factors that integrate the

262 Osteoblast-secreted LCN2 suppresses appetite and decreas

263 analysis of total calvariae versus isolated osteoblasts showed that DKK3, BMP1, vasorin and neogenin

264 e to injury, associated with upregulation of osteoblast-signature genes and activation of canonical W

265 oidal BMSCs differentiate into cortical bone osteoblasts solely during regeneration.

266 and increased trabecular bone mass from pre-osteoblast specific Ezh2 deletion (Ezh2(flox/flox) Osx-C

267 Osteoblast-specific deletion of PPARdelta in mice, in tu

268 e state, while in bone marrow pericytes, the osteoblast-specific gene Runx2 was primed for expression

269 oreover, the impact of postnatally acquired, osteoblast-specific insulin deficiency on the pancreas-t

270 The relationship between osteoblast-specific insulin signaling, osteocalcin activ

271 nesis in MSCs and therefore functioned as an osteoblast-specific marker.

272 SHP2's role in skeletal development, we made osteoblast-specific SHP2 deficient mice using Osterix (O

273 ase activity, and by increased expression of osteoblast-specific transcription factors (eg, runt-rela

274 At the pre-osteoblast stage of differentiation, the locus lost PcG

275 t differentiation and resorption, as well as osteoblast-stimulating 'clastokines'.

276 al and proliferation studies of foetal human osteoblasts subsequently demonstrated good biocompatibil

277 expressed in more-committed Runx2-expressing osteoblasts, Taz does not regulate osteoblast proliferat

278 t of differentiation increased the number of osteoblasts that highly express OPN but not OCN (OPN-OBs

279 l component of a noncanonical ERK pathway in osteoblasts that mediates aberrant ERK activation after

280 ase after mechanical stimulation of a single osteoblast, the model was scaled to a tissue-level injur

281 suggest that FTO functions intrinsically in osteoblasts through Hspa1a-NF-kappaB signaling to enhanc

282 t robustly induces osteopontin expression in osteoblasts through the induction of inhibitor of DNA bi

283 rease exercise capacity, IL-6 must signal in osteoblasts to favor osteoclast differentiation and the

284 ased vasculature and putative chondrocyte to osteoblast transformation dually marked by COL2 and BSP

285 OPN expression in MC3T3-E1 cells and primary osteoblasts treated with differentiation inducers, inclu

286 , simulating mechanotransduction in a single osteoblast under external mechanical perturbations, was

287 odel that overexpresses Jab1 specifically in osteoblasts upon a TP53 heterozygous sensitizing backgro

288 y utilize oxidative phosphorylation, whereas osteoblasts use glycolysis to meet ATP demand.

289 e differentiation of MSCs into adipocytes or osteoblasts using single-cell RNA sequencing, in vitro c

290 nstrate the delivery of a set of PCa-RNAs to osteoblast via PCa-EVs and show the effect on osteoblast

291 Osteocytes communicate with osteoclasts and osteoblasts via distinct signaling molecules that includ

292 e demonstrate that PCa cell EVs both enhance osteoblast viability and produce a significantly more su

293 sdifferentiation into Sertoli-like cells and osteoblasts was attributed in part to the increased recr

294 were inhibited when osteogenesis of affected osteoblasts was driven in the presence of BMP2.

295 in fibroblasts, soft tissue fibroblasts, and osteoblasts were then cultured on regions A, B, and C of

296 rsor cell line (MC3T3-E1) and primary murine osteoblasts were treated with CGS21680, a highly selecti

297 hese cells differentiate to matrix-producing osteoblasts, which form new bone to replace what was res

298 vasorin and neogenin are mainly expressed by osteoblasts, while MIA, LECT1, NGAL and PEDF are express

299 eta-catenin level either in A2AKO mice or in osteoblasts with diminished Akt content.

300 es within these templates persist and become osteoblasts, yet the underlying mechanisms of this proce