ライフサイエンスコーパス: osteocyte

1 e formation and Wnt/beta-catenin activity in osteocytes.

2 onic acid (ZOL), opened Cx43 hemichannels in osteocytes.

3 ion of CCL5 and matrix metalloproteinases in osteocytes.

4 vation was also obtained in isolated primary osteocytes.

5 ore than doubles this zone of dead and dying osteocytes.

6 calized ACVR2A and ACVR2B to osteoblasts and osteocytes.

7 sition, attenuates Saa3 expression in MLO-Y4 osteocytes.

8 required for constitutive Sost expression in osteocytes.

9 s expressed in osteoclasts, osteoblasts, and osteocytes.

10 strongly expressed by osteoblasts and early osteocytes.

11 n is suggested to induce RANKL expression in osteocytes.

12 y on osteoclasts but also on osteoblasts and osteocytes.

13 EGF receptor (EGFR), in both osteoblasts and osteocytes.

14 do ex vivo cultured chondrocytes and primary osteocytes.

15 ed in mice harboring the Notch activation in osteocytes.

16 environment imposed by Gsalpha deficiency in osteocytes.

17 PR40, a receptor expressed on the surface of osteocytes.

18 scape characteristic of primary myocytes and osteocytes.

19 sis, capable of inducing FGF23 production in osteocytes.

20 of markers for chondrocytes, adipocytes, and osteocytes.

21 nvolving activation of the FGFR signaling in osteocytes.

22 with less marrow spaces and well-distributed osteocytes.

23 , becoming embedded in bone matrix as mature osteocytes.

24 dentified as novel markers of differentiated osteocytes.

25 ressive phase stimulates RANKL expression in osteocytes.

26 expression was recently found in osteoblasts/osteocytes.

27 creased loading was lost in mice depleted of osteocytes.

28 ion resulting from loss of WNT1 signaling in osteocytes.

29 come embedded in bone and differentiate into osteocytes.

30 ce to address the role of the GH/IGF axis in osteocytes.

31 of endoplasmic reticulum and mitochondria in osteocytes.

32 anied by positive effects on osteoblasts and osteocytes.

33 of the cell (osteoblast, 12.68% vs. 13.68%; osteocyte, 15.74% vs. 5.37%).

34 whether integrin attachments play a role in osteocyte activation.

35 ated by their capacity to differentiate into osteocytes, adipocytes, and chondrocytes.

36 In conclusion, 17beta-estradiol protects osteocytes against apoptosis by activating the NO/cGMP/P

37 nent of the mechanotransduction machinery in osteocytes, albeit beta-catenin/T cell factor-mediated t

38 or osteoclastogenesis, our data suggest that osteocytes also produce IFN-beta as an inhibitor of oste

39 n the number of activated caspase-3-positive osteocytes among groups and time points.

40 Osteocyte and osteocyte lacuna counts, percent bone matr

41 hrombotic occlusion, marrow fat hypertrophy, osteocyte and/or endothelial cell apoptosis, hypercoagul

42 respective precursor cells, with the role of osteocytes and bone lining cells left largely unexplored

43 real time and quantified Ca(2+) responses in osteocytes and bone surface cells in situ under controll

44 tors produce CD146(+), CD166(+) progenitors, osteocytes and CXCL12-producing stromal cells.

45 steocytes as assessed by RNA-seq in cultured osteocytes and following in vivo administration.

46 T gene, is produced postnatally primarily by osteocytes and is a negative regulator of bone formation

47 r of nuclear factor-kappaB ligand (RANKL) in osteocytes and mouse calvarial explants and preferential

48 Importantly, direct contact between osteocytes and multiple myeloma cells reciprocally activ

49 acterize the local mechanical environment of osteocytes and osteoblasts from healthy and osteoporotic

50 Apoptosis of osteocytes and osteoblasts precedes bone resorption and

51 sis of gene expression in mouse osteoblasts, osteocytes and osteoclasts.

52 signals, including osteoblasts, osteoclasts, osteocytes and osteoprogenitors.

53 cellular protein preferentially expressed by osteocytes and periosteal osteoblasts in response to mec

54 gen control of B cell number is indirect via osteocytes and that the increase in bone marrow B cells

55 tinct roles of ATP and adenosine released by osteocytes and the activation of corresponding receptors

56 tion of mesenchymal stem cells, osteoblasts, osteocytes, and chondrocytes.

57 spectively, p<0.01), with MMP10 localized to osteocytes, and consistent with induction of osteocytic

58 subsets of these stromal cells, osteoblasts, osteocytes, and hypertrophic chondrocytes secrete a C-ty

59 nsive hyperosteoidosis, also surrounding the osteocytes, and hypomineralization of the entire bone co

60 ecular thinning, higher numbers of apoptotic osteocytes, and imbalanced metabolism, leading to defect

61 ticoids (GCs) have been shown to induce both osteocyte apoptosis and autophagy, we sought to determin

62 nhibit resorption, prevented the increase in osteocyte apoptosis and osteocytic RANKL expression.

63 d that pioglitazone and rosiglitazone induce osteocyte apoptosis and sclerostin up-regulation; howeve

64 Activation of this pathway led only to osteocyte apoptosis but not sclerostin up-regulation.

65 the importance of changes in osteoclast and osteocyte apoptosis in response to estrogen deficiency a

66 These results demonstrate that osteocyte apoptosis leads to increased osteocytic RANKL.

67 Mechanistic studies revealed that osteocyte apoptosis was initiated by multiple myeloma ce

68 hway led to sclerostin up-regulation but not osteocyte apoptosis.

69 Osteocytes are bone cells that form cellular networks th

70 Osteocytes are considered to be the major mechanosensory

71 s in individual osteoblasts, osteoclasts and osteocytes are limited and impair our ability to assess

72 Because osteocytes are major RANKL producers, we hypothesized th

73 Osteocytes are master orchestrators of bone remodeling;

74 Osteocytes are terminally differentiated osteoblasts emb

75 Osteocytes are the most abundant but least understood ce

76 Osteocytes are the terminally differentiated cell type o

77 Connexin (Cx) 43 hemichannels in osteocytes are thought to play a critical role in releas

78 Living inhabitants of the hip bone (e.g. osteocytes) are visible in their local extracellular mat

79 Sclerostin and DKK1, both secreted mainly by osteocytes, are important Wnt inhibitors and as such can

80 lling tools created a zone of dead and dying osteocytes around the osteotomy.

81 tumor microenvironment, and they identified osteocytes as a critical mediator in the bone metastatic

82 this work identifies an anabolic function of osteocytes as a source of Wnt in bone development and ho

83 ibition mimics many of the effects of PTH in osteocytes as assessed by RNA-seq in cultured osteocytes

84 d signaling of osteoclasts, osteoblasts, and osteocytes, as well as proliferation and differentiation

85 glucocorticoid signalling in osteoblasts and osteocytes attenuates murine experimental arthritis.

86 capable of localized repair even without the osteocytes believed essential for this process.

87 Despite progress in understanding osteocyte biology and function, much remains to be eluci

88 Osteocytes, but not surface cells, displayed repetitive

89 trated that both stimuli promote survival of osteocytes by activating the ERKs.

90 itionally deleted Pkd1 in mature osteoblasts/osteocytes by crossing Dmp1-Cre with Pkd1(flox/m1Bei) mi

91 h1 and -2 were inactivated preferentially in osteocytes by mating Notch1/2 conditional mice, where No

92 intracellular Ca(2+) responses of individual osteocytes by using a genetically encoded fluorescent Ca

93 It is known that osteocytes can sense changes in bone strain.

94 r Atg7, a gene essential for autophagy, from osteocytes caused low bone mass in 6-month-old male and

95 ent to which focal mechanical stimulation of osteocyte cell body and process led to activation of the

96 newton-level mechanical loading, whereas the osteocyte cell body and processes with no local attachme

97 nd autophagy, we sought to determine whether osteocyte cell fate in the presence of GCs was dose depe

98 e regions of periodic attachment between the osteocyte cell membrane and its canalicular wall are sit

99 s for the possibility of RANKL expression by osteocyte cell populations.

100 ins at localized attachment sites around the osteocyte cell process.

101 Conditioned media (CM) collected from MLO-Y4 osteocyte cells treated with bisphosphonates inhibited t

102 nsidered to be initiated and orchestrated by osteocytes, cells within the bone matrix.

103 sion of autophagy also reduced the amount of osteocyte cellular projections and led to retention of e

104 Matrix-embedded osteocytes comprise more than 95% of bone cells and are

105 , late osteoblastic MLO-A5 cells, and MLO-Y4 osteocytes, consistent with findings using primary bone

106 RKO upon PTH administration, indicating that osteocytes control osteoclast formation through a PPR-me

107 Hence, osteocytes coregulate bone and glucose homeostasis throu

108 cer cells were mediated by ATP released from osteocyte Cx43 hemichannels.

109 data also suggest that reducing the zone of osteocyte death will improve osteotomy site viability, l

110 ructure, characterized by widespread loss of osteocytes, defects in mineralization, and a hypocellula

111 tivation of the UPR in early differentiating osteocytes delays maturation, maintaining active bone sy

112 Bone microstructure was evaluated for osteocyte density (OD), bone vessel volume density (BVVD

113 zing antibody, indicating a critical role of osteocyte-derived G-CSF in the myeloid expansion.

114 Elevated plasma levels of the osteocyte-derived hormone fibroblast growth factor 23 (F

115 Sclerostin is an osteocyte-derived inhibitor of osteoblast activity.

116 However, Ca(2+) intensity within responding osteocytes did not change significantly with physiologic

117 tional hemichannels but not gap junctions in osteocytes did not display a significant difference.

118 ERalpha in mature osteoblasts or osteocytes did not influence cancellous or cortical bone

119 aken together, the miR-23a cluster regulates osteocyte differentiation by modulating the TGF-beta sig

120 pproximately 24-2 (miR-23a cluster) promotes osteocyte differentiation.

121 em cells and in vitro-generated myocytes and osteocytes display a significantly different DNA methylo

122 g ERalpha protein expression specifically in osteocytes (Dmp1-ERalpha(-/-)).

123 To activate Notch preferentially in osteocytes, Dmp1-Cre transgenics were crossed with Rosa(

124 Therefore, osteocytes do not mediate the HSC expansion induced by P

125 strate that activation of PTH1R signaling in osteocytes does not expand BM HSCs, which are instead de

126 Here, we find that suppression of osteocyte-driven perilacunar remodeling, a fundamental c

127 utonomous increase in Fgf23 secretion in Hyp osteocytes drives the accumulation of pyrophosphate thro

128 called perilacunar remodeling, bone-embedded osteocytes dynamically resorb and replace the surroundin

129 anotransduction phenomenon holds for in situ osteocytes embedded within a mineralized bone matrix und

130 Conditioned media from osteocyte-enriched bone explants significantly increased

131 ocytes, we prepared non-osteocytic cell-free osteocyte-enriched bone fragments (OEBFs).

132 g at the trabecular surfaces and in cortical osteocytes, epiphyseal chondrocytes, marrow adipocytes a

133 5 coreceptor specifically in osteoblasts and osteocytes exhibit the expected reductions in postnatal

134 In vitro studies have shown that osteocytes exhibited unique calcium (Ca(2+)) oscillation

135 In healthy bone tissue, osteocytes experience higher maximum strains (31,028 +/-

136 modeling (i.e. osteoblasts, osteoclasts, and osteocytes) express LPA1, but delineating the role of th

137 ting osteoporotic patients despite increased osteocyte-expressed RANKL.

138 to the morphological changes associated with osteocyte formation.

139 Sclerostin was expressed in osteocytes from bones from naive and myeloma-bearing mic

140 the factors that regulate differentiation of osteocytes from mature osteoblasts are poorly understood

141 mone both in vitro and in vivo, and protects osteocytes from oxidative stress.

142 Carbonic anhydrase III protects osteocytes from oxidative stress.

143 TG osteocytes had no increase in signals associated with mi

144 Recently, the role of osteocytes has been frequently addressed, with focus on

145 Osteocytes have a role in sensing and translating mechan

146 Osteocytes have been hypothesized to be the major mechan

147 ilt, stromal cells including fibroblasts and osteocytes have their own independent immunologic functi

148 /f) mice, in which SOCS3 has been ablated in osteocytes, have high trabecular bone volume and poorly

149 t group of specialized cells, also including osteocytes, hypertrophic chondrocytes, and odontoblasts.

150 resultant fluid-induced shear stress on the osteocyte in the lacunocanalicular system (LCS) was also

151 r in cementum in comparable fashion with the osteocyte in the skeleton, responding to changing tooth

152 Here, we report that osteocytes in a mouse model of human MM physically inter

153 y induced CCL7 may be to selectively protect osteocytes in an autocrine manner against glucocorticoid

154 y of the qualitative features of the role of osteocytes in bone biology as presented in recent litera

155 ngs challenge the unique and primary role of osteocytes in bone remodeling, a basic tenet of bone bio

156 Furthermore, osteocytes in contact with multiple myeloma cells expres

157 r RANKL (TNFSF11) and sclerostin levels than osteocytes in control mice.

158 ffect of estrogen is mediated via ERalpha in osteocytes in males, but via ERalpha in osteoclasts in f

159 e-derived bone cells to form osteoblasts and osteocytes in metaphyses.

160 y results in a narrow zone of dead and dying osteocytes in peri-implant bone that is not significantl

161 CCL7 was increased in osteocytes in response to tooth movement in vivo.

162 two distinct signaling pathways activated in osteocytes in response to TZDs that could participate in

163 ings are consistent with the hypothesis that osteocytes in situ are highly polarized cells, where mec

164 Osteocytes in the lacunar-canalicular system of the bone

165 uce measures of Wnt/beta-catenin activity in osteocytes in the loaded bone.

166 cal role of connexin (Cx) 43 hemichannels in osteocytes in the suppression of breast cancer bone meta

167 nical stimulation has been widely studied in osteocytes in vitro and in bone explants, but has yet to

168 major mechanosensory cells of bone, but how osteocytes in vivo process, perceive, and respond to mec

169 equencies examined, the number of responding osteocytes increased strongly with applied strain magnit

170 In contrast, Notch activation in osteocytes increases bone mass, but the mechanisms invol

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

172 Wnt/Lrp5 signaling regulates osteoblasts and osteocytes, introduce new players in Wnt signaling pathw

173 Therefore, a major arm of PTH signalling in osteocytes involves SIK inhibition, and small molecule S

174 Cx43) hemichannel (HC) in the mechanosensory osteocytes is a major portal for the release of factors

175 Here, we examined whether RANKL produced by osteocytes is also required for the bone loss caused by

176 orption induced by PTH receptor signaling in osteocytes is critical for full anabolism in cortical bo

177 vator of NFkappaB ligand (RANKL) produced by osteocytes is essential for osteoclast formation in canc

178 We hypothesized that ERalpha in osteocytes is important for trabecular bone in male mice

179 Mechanistically, Saa3 produced by MLO-Y4 osteocytes is integrated into the extracellular matrix o

180 r bone remodeling, and receptor signaling in osteocytes is needed for anabolic and catabolic skeletal

181 r, these data indicate that PPR signaling in osteocytes is required for bone remodeling, and receptor

182 results demonstrate that RANKL expressed by osteocytes is required for the bone loss as well as the

183 we report that CAIII is highly expressed in osteocytes, is regulated by parathyroid hormone both in

184 Osteocyte and osteocyte lacuna counts, percent bone matrix loss, and f

185 remodeling while causing degeneration of the osteocyte lacunocanalicular network, collagen disorganiz

186 cept for a sharp increase in osteoblasts and osteocytes, leading to a profound increase in bone volum

187 al deletion of Mbtps1 (cKO) protease in bone osteocytes leads to an age-related increase in mass (12%

188 sis, while its ablation by CRISPR/Cas9 in an osteocyte-like cell line (Ocy454) enhanced it.

189 Using an osteocyte-like cell line along with in vivo studies, we

190 Murine cementoblasts (OCCM-30) and osteocyte-like cells (MLO-Y4 and MLO-A5), known to expre

191 Tnap expression is decreased in Hyp-derived osteocyte-like cells but not in Hyp-derived osteoblasts

192 d pyrophosphate concentration in Hyp-derived osteocyte-like cells in vitro.

193 In contrast, in Osmr(-/-) primary osteocyte-like cells stimulated with mOSM (therefore act

194 Etoposide-induced death of MLO-Y4 osteocyte-like cells, assessed by trypan blue staining,

195 d enzyme enriched in primary cilia of MLO-Y4 osteocyte-like cells, may play a role in a primary ciliu

196 ctic myokine, was highly expressed in MLO-Y4 osteocyte-like cells.

197 n of mature osteoblasts into matrix-embedded osteocytes likely contributed to depletion of the osteob

198 Additionally, they influence the survival of osteocytes, long-lived cells that are entombed within th

199 pronouncedly in mice deficient in osteoblast/osteocyte Lrp4, consistent with our observation in human

200 s accompanied by decreased expression of the osteocyte marker and Wnt-signaling inhibitor sclerostin,

201 tin matrix protein-1 (DMP1, a mechanosensory/osteocyte marker), while osteoblast markers, bone sialop

202 ll reduced, that of cyclin-dependent kinase, osteocyte marker, and pro-apoptotic genes were increased

203 had reduced expression of several osteoblast/osteocyte markers in bone, including Runx2, Sp7, and Dmp

204 remarkably high bone turnover and defective osteocyte maturation that is accompanied by decreased ex

205 Whereas osteocytes may produce CCL2 in constitutively low levels

206 e in a primary cilium-dependent mechanism of osteocyte mechanotransduction in vitro.

207 rimary cilia and AC6 in a novel mechanism of osteocyte mechanotransduction.

208 Thus, osteocyte-mediated perilacunar remodeling maintains bone

209 To establish whether osteocyte-mediated PTH1R signaling expands HSCs, we stud

210 demonstrate that suppression of autophagy in osteocytes mimics, in many aspects, the impact of aging

211 This work extends the understanding of how osteocytes modulate their microenvironment in response t

212 and bone disease, suggesting that targeting osteocyte-multiple myeloma cell interactions through spe

213 d protein expression was reduced in cKO bone osteocytes, no differences in Mbtps1 or cre recombinase

214 The vital canalicular networks required for osteocyte nourishment and communication, as well as the

215 ion rate were significantly reduced, whereas osteocyte number was increased.

216 ated with decreased osteoblast but increased osteocyte numbers.

217 or miR-27a, but not miR24-2, show decreased osteocyte numbers.

218 goal, we generated mice with PPR deletion in osteocytes (Ocy-PPRKO).

219 e next proved that the pathologic changes in osteocytes (Ocys; changes from a spindle shape to round

220 mice rescued the suppressed TNAP activity in osteocytes of Hyp mice.

221 beta-Galactosidase activity was detected in osteocytes of sost KO mice but was undetectable in WT mi

222 body weight activates a sensor dependent on osteocytes of the weight-bearing bones.

223 roles of ATP and adenosine released by bone osteocytes on breast cancers.

224 ce lacking Lrp4 in osteoblasts/osteocytes or osteocytes only.

225 e generated mice lacking Lrp4 in osteoblasts/osteocytes or osteocytes only.

226 e lacking these receptors in osteoblasts and osteocytes (osteocalcin-Cre).

227 Osteoclastogenesis is controlled by osteocytes; osteocytic osteoclastogenesis regulatory mol

228 Correlation between osteocytes per lacuna and age at death may reflect repor

229 osteocytes results in the loss of the mature osteocyte phenotype.

230 ith increased cellular maturation toward the osteocyte phenotype.

231 However, there is increasing evidence that osteocytes play important roles in the cycle of targeted

232 he essential role of alphaVbeta3 integrin in osteocyte-polarized mechanosensing and mechanotransducti

233 together with disrupted trabeculae, loss of osteocytes, presence of calcified marrow, and elevated e

234 er, we showed that Ca(2+) signaling from the osteocyte process to the cell body was greatly diminishe

235 Our results indicate that osteocyte processes are extremely responsive to piconewt

236 luid stimulus probe to hydrodynamically load osteocyte processes vs. cell bodies in murine long bone

237 ta suggest that inhibitors of sclerostin, an osteocyte-produced Wnt signaling pathway antagonist, can

238 Importantly, these osteocytes recapitulated the in vivo response to mechani

239 In conclusion, ERalpha in osteocytes regulates trabecular bone formation and there

240 gamma expression in bone cells, particularly osteocytes, regulates energy metabolism remains unknown.

241 quired for osteoblasts to differentiate into osteocytes--remain a matter of conjecture with several h

242 physiological relevance of PPR signaling in osteocytes remains to be elucidated.

243 This study provides direct evidence that osteocytes respond to in situ mechanical loading by Ca(2

244 How in situ osteocytes respond to mechanical stimuli is still unclea

245 Osteocyte responses are imaged by using multiphoton fluo

246 Deletion of Wnt1 in osteocytes resulted in low bone mass with spontaneous fr

247 Depletion of Saa3 in MLO osteocytes results in the loss of the mature osteocyte p

248 of bone remodeling that includes the role of osteocytes, sclerostin, and allows for the possibility o

249 s also increasing interest in sclerostin, an osteocyte-secreted bone formation inhibitor, and its rol

250 Sclerostin is an osteocyte-secreted soluble antagonist of the Wnt/beta-ca

251 , vascular calcification, and stimulation of osteocyte secretion.

252 Mice lacking Gsalpha in osteocytes showed a dramatic increase in myeloid cells i

253 KL producers, we hypothesized that apoptotic osteocytes signal to neighboring osteocytes to increase

254 duced to differentiate into chondrocytes and osteocytes soon began to express and secrete YKL-40 prot

255 Here, we show that mature osteoblast/osteocyte-specific ablation of PPARgamma in mice (Ocy-PP

256 ng ECR5 or Mef2C through Col1-Cre osteoblast/osteocyte-specific ablation result in high bone mass (HB

257 th Cx43 osteocyte-specific knockout mice and osteocyte-specific Delta130-136 transgenic mice with imp

258 nces bone properties, we generated mice with osteocyte-specific expression of inducible Lrp5 mutation

259 Furthermore, both Cx43 osteocyte-specific knockout mice and osteocyte-specific

260 heretofore unrecognized factors, such as the osteocyte-specific protein sclerostin, also regulate ren

261 Interestingly, assessment of the osteocyte-specific RANKL/OPG ratio showed that the stero

262 Sclerostin is an osteocyte-specific Wnt antagonist that inhibits bone for

263 m, we generated late-osteoblast-specific and osteocyte-specific WNT1 loss- and gain-of-function mouse

264 Conversely, Wnt1 overexpression from osteocytes stimulated bone formation by increasing osteo

265 " the osteocytes, where insights gained from osteocyte studies serve to inform the critical examinati

266 ed the expression of the gene in a subset of osteocytes, suggesting the presence of altered cross-tal

267 g that most extant fishes (neoteleosts) lack osteocytes, suggesting their bones are not constantly re

268 ns promote bone health in part by increasing osteocyte survival, an effect that requires activation o

269 n pathways in mechanotransduction leading to osteocyte survival.

270 in the transduction of mechanical cues into osteocyte survival.

271 NO/cGMP signaling in estrogen regulation of osteocyte survival.

272 expressing a constitutively active PTH1R in osteocytes (TG mice).

273 ice with activated PTH receptor signaling in osteocytes that exhibit increased bone mass and remodeli

274 ion is under the control of WNT1 produced by osteocytes, the cells that reside deep in the bone matri

275 Application of pressure to osteocytes, the main mechanotransducing cells in bone, i

276 Osteocytes, the most abundant bone cells, were shown to

277 Osteocytes, the most abundant cells in adult bone, also

278 Osteocytes, the most abundant yet least understood cells

279 Thus, targeted osteocyte therapies could hold promise as novel osteopor

280 Despite lacking osteocytes, this tissue exhibits a striking resemblance

281 sed parathyroid hormone levels, we subjected osteocytes to an in vitro unloading environment achieved

282 kl/Opg (TNFRSF11B) ratio, and the ability of osteocytes to attract osteoclast precursors to induce lo

283 t apoptotic osteocytes signal to neighboring osteocytes to increase RANKL expression, which, in turn,

284 altering the sensitivity of osteoblasts and osteocytes to mechanical signals.

285 thyroid hormone (PTH) activates receptors on osteocytes to orchestrate bone formation and resorption.

286 We investigated the in vivo responses of osteocytes to strains ranging from 250 to 3,000 [Formula

287 ocally regulated with Saa3 at the osteoblast/osteocyte transition, attenuates Saa3 expression in MLO-

288 d that conditioned media (CM) collected from osteocytes treated with alendronate (AD), a bisphosphona

289 In conclusion, Notch plays a unique role in osteocytes, up-regulates osteoprotegerin and Wnt signali

290 ed a ~70-fold up-regulation of Fgfr3 mRNA in osteocytes versus osteoblasts of Hyp mice.

291 ntiation into chondrocytes, osteoblasts, and osteocytes via the BMP4-pSMAD5 and COX-2-PGE2 signaling

292 Osteocyte viability is a critical determinant of bone st

293 ss of strength, suggesting a contribution of osteocyte viability to strength independent of bone mass

294 loading plays a crucial role in maintaining osteocyte viability, CCL7 was tested for protective acti

295 ANKL) and osteoprotegerin (OPG) signaling in osteocytes was not studied in sheep.

296 factors up-regulated by mechanical strain in osteocytes, we discovered that chemokine (C-C motif) lig

297 To study primary osteocytes, we prepared non-osteocytic cell-free osteocy

298 Mice lacking RANKL in osteocytes were protected from the increase in osteoclas

299 mparing them to their closest "cousins," the osteocytes, where insights gained from osteocyte studies

300 rocesses vs. cell bodies in murine long bone osteocyte Y4 (MLO-Y4) cells with physiological-level for