ライフサイエンスコーパス: calvarial

1 mRNA level was highly elevated in Ank(KI/KI) calvarial and femoral bones.

2 In both primary rat calvarial and MC3T3E1 mouse calvarial osteoblasts, trans

3 accumulated on the endosteal surface in the calvarial and trabecular bone marrow.

4 Analysis of calvarial- and bone marrow-derived osteoblasts for miner

5 requirement is restricted to the developing calvarial aspect of the frontal bone, whereas the orbita

6 Using a calvarial bone defect model in rats, it was shown that P

7 phate/hydroxyapatite scaffold implanted in a calvarial bone defect, promoted significantly more bone

8 variety of pathological conditions in which calvarial bone development is compromised.

9 Runx2 is essential for calvarial bone development, as Runx2 haploinsufficiency

10 ction for both the CNC- and mesoderm-derived calvarial bone development.

11 precursor cells and the rate and pattern of calvarial bone development.

12 eoblast differentiation, mineralization, and calvarial bone development.

13 eased ALP activity and osteocalcin levels of calvarial bone extracts.

14 purified from conditioned medium stimulated calvarial bone formation and induced osteoblast differen

15 mvastatin has been shown to stimulate murine calvarial bone growth after multiple injections.

16 osteogenic fronts is the main mechanism for calvarial bone growth, but importantly, we show that sut

17 at suture mesenchyme cells can contribute to calvarial bone growth.

18 nitor cell population determines the rate of calvarial bone growth.

19 Mice lacking En1 exhibit generalized calvarial bone hypoplasia and persistent widening of the

20 microscopy to perform imaging studies of the calvarial bone marrow (BM) of xenografted mice, we show

21 ription factor that controls ossification in calvarial bone of the developing skull.

22 We have utilized our unique live mouse calvarial bone organ culture models under conditions whi

23 e resorption model using live mouse neonatal calvarial bone organ cultures stimulated by parathyroid

24 After 12 weeks, calvarial bone regeneration was evaluated radiographical

25 (TNF) activities only partially account for calvarial bone resorption induced by local application o

26 o, in a mouse model of P. gingivalis-induced calvarial bone resorption, injection of mmu-miR-155-5p o

27 r confirmed in osteoprogenitors close to the calvarial bone surface.

28 These hypomorphic mice have altered calvarial bone volume, as observed by histology and micr

29 e intravital imaging studies using a chronic calvarial bone window showed that our QD-Ab conjugates d

30 athogen Porphyromonas gingivalis adjacent to calvarial bone with or without prior immunization agains

31 ties of the ITOP by fabricating mandible and calvarial bone, cartilage and skeletal muscle.

32 structures--such as the mandibular condyle, calvarial bone, cranial suture, and subcutaneous adipose

33 Furthermore, anomalies were restricted to calvarial bone, despite generalized, non-tissue-specific

34 (P = 0.02) increase at the thickest point of calvarial bone, while MEM-SIM caused a highly significan

35 fferentiation and bone formation in cultured calvarial bone.

36 As the calvarial bones advance to envelop the brain, fibrous su

37 ellular mechanisms control the growth of the calvarial bones and conversely, what is the fate of the

38 rder that results in the premature fusion of calvarial bones and ensuing abnormalities in skull shape

39 blation of Tbx1 affected Runx2 expression in calvarial bones and overexpression of Tbx1 induced Runx2

40 n bone resorption in cultured neonatal mouse calvarial bones and their interaction with glucocorticoi

41 e fate of the sutural mesenchymal cells when calvarial bones approximate to form a suture.

42 testify that their headache feels as if the calvarial bones are deformed, crushed, or broken.

43 This has lead us to postulate that the calvarial bones are supplied by sensory fibers.

44 TNF administration over calvarial bones caused decreases in Smad1 and Runx2 prot

45 stimulated by ATRA was also blocked by GC in calvarial bones from mice with a GR mutation that blocks

46 raniosynostosis, the premature fusion of the calvarial bones of the skull, is a relatively common ped

47 s that serve as growth centers and allow the calvarial bones to expand as the brain enlarges.

48 Exposure of calvarial bones to GC inhibited the stimulatory effects

49 he broadly expressed CMV promoter causes the calvarial bones to invade the sagittal suture.

50 ostosis, the premature fusion of one or more calvarial bones with consequent abnormalities in skull s

51 alyses showed defective dentin, alveolar and calvarial bones, and sutures during development.

52 increased uptake were also detected in other calvarial bones, in several vertebras and in the proxima

53 mal spinal curvatures, and dysmorphic facial/calvarial bones, similar to the human phenotype.

54 fferentiation of osteoblasts, which form the calvarial bones.

55 lastic cells in the osteogenic fronts of the calvarial bones.

56 defect characterized by premature fusion of calvarial bones.

57 inoic acid stimulated release of (45)Ca from calvarial bones.

58 tors (RARalpha/beta/gamma) were expressed in calvarial bones.

59 cible Cre-ER-mediated ALK5-deficient primary calvarial cell cultures, we found that TGF-beta signalin

60 Moreover, fetal rat osteogenic calvarial cells (FOCCs) from these obese dams have signi

61 Re-plating assays of primary RB1(-/-) calvarial cells after differentiation showed a clear adi

62 Using primary calvarial cells and explants, C3H10T1/2 cells, and C2C12

63 entiation after transfection into Runx2-null calvarial cells and mesenchymal cells.

64 GF expression was down-regulated in Osx-null calvarial cells and that osteoblast marker osteocalcin e

65 Calvarial cells but not embryonic fibroblasts from Runx2

66 Reintroduction of Runx2 into Runx2(-/-) calvarial cells by adenoviral delivery restores stringen

67 Consistently, Cpdm primary calvarial cells display reduced osteogenic capacity ex v

68 Finally, cultured Ku70 -/- calvarial cells exhibit a profound, selective deficiency

69 els of Runx2, Col1, and OPN identified using calvarial cells from DSPP-null and wild-type mice in an

70 ted in ex vivo cell culture of primary fetal calvarial cells from p47(phox-/-) mice.

71 was suppressed by ENPP1-specific shRNA, and calvarial cells isolated from Enpp1 knock-out mice show

72 First, in calvarial cells of embryonic day (E)18.5 Osx-null embryo

73 n both bone marrow stromal cells (BMSCs) and calvarial cells of mutant mice.

74 ivo overexpression of RCAS-Dlx5WT in BSP/TVA calvarial cells promoted, whereas that of RCAS-Dlx5RH in

75 n osteogenesis, and that in primary RB1(-/-) calvarial cells there is an increased osteoprogenitor po

76 When rat primary calvarial cells were cultured on the scaffolds in biorea

77 Axin2 levels are elevated in Runx2(-/-) calvarial cells, and Runx2 represses transcription of Ax

78 c differentiation of C2C12 cells and primary calvarial cells, and suppression of this endogenous expr

79 asts accelerated in vitro differentiation of calvarial cells, as well as in vivo bone development, wh

80 in OC expression as compared with wild-type calvarial cells, confirming the biochemical data showing

81 dipogenic potential to immortalized RB1(+/+) calvarial cells, suggesting that these traits are not a

82 verexpression/knockdown studies in fetal rat calvarial cells, we show that thiazides increase the for

83 Golgi and plasma membrane fractions of mouse calvarial cells.

84 on in vitro differentiation of primary mouse calvarial cells.

85 1 endocytosis in pre-osteoblasts and primary calvarial cells.

86 lateral cerebellar atrophy, and compensatory calvarial changes.

87 yostatin deficiency altered fetal growth and calvarial collagen content of newborn mice and conferred

88 Type I calvarial collagen isolated from these mice showed reduc

89 The materials were placed into 8-mm calvarial critical-size defects (CSD).

90 treatment groups and anesthetized, and 8 mm calvarial critical-sized defects were created.

91 ed bone cell populations at days 7 and 17 of calvarial cultures revealed an increased specificity reg

92 In calvarial cultures we reduced osteoprogenitor cell proli

93 atic enhancement of bone formation in intact calvarial cultures.

94 profiles were evaluated in a critical-sized calvarial defect model in rats.

95 able of regenerating bone in a critical size calvarial defect model when transduced with BMP 2 or 4;

96 bone regeneration utilizing a critical size calvarial defect model.

97 e-dimensional settings as well as in a mouse calvarial defect model.

98 te bone formation in a murine critical-sized calvarial defect model.

99 y improved BMMSC-based bone regeneration and calvarial defect repair in C57BL/6 mice.

100 wise to a silk scaffold and applied to a rat calvarial defect.

101 ibe the protocol for one such model, the rat calvarial defect.

102 gates were implanted into rat critical-sized calvarial defects (CSD).

103 nsplants were introduced into critical-sized calvarial defects and contralateral control skull defect

104 cally enhanced the healing of critical-sized calvarial defects and increased both bone volume fractio

105 n transduced WT MDSCs when transplanted into calvarial defects created in CD-1 nude mice.

106 r transplanting MDSCs into the critical-size calvarial defects created in normal mice, we found that

107 alone or with endothelial cells into 8.5-mm calvarial defects created in nude rats.

108 to radio-opacity of microscopically ossified calvarial defects filled with fibroblast-free, BMP2-load

109 lly transduced BLK cells into critical-sized calvarial defects generated in C57BL6 mice.

110 To test this hypothesis, we created 40 calvarial defects in 20 12-week-old New Zealand White ra

111 were also investigated using critical-sized calvarial defects in mice repaired with noggin-suppresse

112 erimental) were implanted in two midsagittal calvarial defects in the parietal bone.

113 ted new bone formation to heal critical-size calvarial defects in vivo.

114 of the knee joints of experimental rats and calvarial defects of Jax mice.

115 ells; P = .02 and P = .04, respectively) and calvarial defects of recipient mice (mean, 21.7 msec vs

116 ell-1 protein-coated PLGA scaffolds into rat calvarial defects revealed the osteogenic potential of N

117 aseous ozone on bone healing in diabetic rat calvarial defects treated with xenografts.

118 Most Msx2-mutant phenotypes, including calvarial defects, are enhanced by genetic combination w

119 collagen-producing cells resulted in severe calvarial defects, decreased bone size, bone mineral den

120 into experimentally induced nonself healing calvarial defects, GW treatment substantially increased

121 dura mater cells to heal critical-size mouse calvarial defects.

122 but not adult, osteoblasts successfully heal calvarial defects.

123 n alloplast on the healing of critical-sized calvarial defects.

124 osteoblastic and keratinocyte cell lines and calvarial derived osteoblasts in which the expression of

125 rived adult stromal (ADAS) cells, BMS cells, calvarial-derived osteoblasts and dura mater cells to he

126 with bone marrow stromal cells and juvenile calvarial-derived osteoblasts.

127 ls having a better progenitor potential than calvarial-derived stromal cells.

128 panding and differentiating abilities during calvarial development and homeostastic maintenance.

129 Ps) correlated with key events in post-natal calvarial development and MC3T3 cell mineralization.

130 le-suture synostosis; by contrast, embryonic calvarial development appears mildly delayed.

131 s thus identify a novel mechanism underlying calvarial development in craniosynostosis.

132 he neural crest results in severe defects in calvarial development, although the cellular and molecul

133 have important regulatory roles in postnatal calvarial development.

134 s suggest that Msx genes have a dual role in calvarial development: They are required for the differe

135 d post-natal growth regulation of individual calvarial elements.

136 appaB ligand (RANKL) in osteocytes and mouse calvarial explants and preferentially induces apoptosis

137 In the current study, cultured calvarial explants isolated from Nell-1 transgenic newbo

138 Osteoblasts from both stromal and calvarial explants showed delayed maturation in vitro as

139 We trace the origin of the calvarial foramen defect in Msx2 mutant mice to a group

140 defects of skull ossification and persistent calvarial foramen.

141 tations in MSX2 and TWIST are known to cause calvarial foramina in humans.

142 One such anomaly is familial calvarial foramina, persistent unossified areas within t

143 Expansion of the brain is coupled with calvarial growth through a series of tissue interactions

144 s by combining their understanding of normal calvarial growth with a careful physical examination.

145 their ability to induce bone formation in a calvarial induction assay.

146 anial neural crest (CNC) and consists of the calvarial (lateral) aspect that covers the frontal lobe

147 Mineralization density was reduced in calvarial, maxillary, and mandibular alveolar bone follo

148 A reduction in calvarial membranous bone deposition and mineralization

149 sion pattern of FGF ligands and receptors of calvarial mesenchymal cells during their own osteogenic

150 ), and Bmp2 are expressed ectopically in the calvarial mesenchyme, which results in aberrant osteobla

151 s, including dental abnormalities, deficient calvarial mineralization, and reduced bone mass.

152 is was accomplished by the use of an in vivo calvarial model in mice with targeted deletion of TNF re

153 connective tissue, we used a well-documented calvarial model to study host-bacterium interactions.

154 Utilizing a murine calvarial model, Mk2(+/+) and Mk2(-/-) mice were treated

155 ure mesenchyme serves as a growth centre for calvarial morphogenesis and has been postulated to act a

156 eoprogenitors at the osteogenic front during calvarial morphogenesis, and closely resembles that asso

157 Calvarial OBs were cultured in the presence of MKs for v

158 Mouse calvarial organ culture revealed that EGF elevated the n

159 ith these data, addition of IL-7 to neonatal calvarial organ cultures blocked new bone formation, and

160 tion in both mesenchymal stem cell lines and calvarial organ cultures.

161 f immature animals to orchestrate successful calvarial ossification has been well described.

162 oreactors and 3D scaffolds for culturing rat calvarial osteoblast cells.

163 ssed during the proliferative phase of mouse calvarial osteoblast cultures but was preferentially dow

164 Primary calvarial osteoblast cultures demonstrated that the 2.5

165 Primary calvarial osteoblast cultures derived from 5- to 7-day-o

166 is of Amel- and Ambn-deficient calvariae and calvarial osteoblast cultures revealed a dramatic reduct

167 Primary mouse calvarial osteoblast cultures were established and inocu

168 way in the bone collar as well as in primary calvarial osteoblast cultures.

169 in the UMR cells, but was reduced in the rat calvarial osteoblast cultures.

170 The calvarial osteoblast development is significantly affect

171 In vitro, Nell-1 overexpression accelerated calvarial osteoblast differentiation and mineralization

172 study identifies EN1 as a novel modulator of calvarial osteoblast differentiation and proliferation,

173 , an autocrine canonical Wnt, during primary calvarial osteoblast differentiation revealed that scler

174 s total lipids and lipid fractions inhibited calvarial osteoblast gene expression and function in viv

175 h factors (FGFs) are important regulators of calvarial osteoblast growth and differentiation.

176 e effects of FGF treatment on primary murine calvarial osteoblast, and on OB1, a newly established os

177 th a more osteogenic differentiated state of calvarial osteoblast.

178 R 106-01 osteosarcoma cells, and primary rat calvarial osteoblastic cells also express another gap ju

179 reduced approximately 40-50% in fetal mouse calvarial osteoblastic cells exposed to 1% ethanol for 4

180 by FGF2 in phenotypically immature MC3T3-E1 calvarial osteoblastic cells.

181 eralization of bone nodules in primary mouse calvarial osteoblastic cultures was completely blocked b

182 Murine calvarial osteoblasts (MOBs) were grown in OST medium fo

183 However, when calvarial osteoblasts (OBs) were isolated from neonatal

184 high levels in testis and at lower levels in calvarial osteoblasts and brain.

185 velopment of the osteoblast phenotype in rat calvarial osteoblasts and in proliferating and growth-in

186 l studies, and ex vivo differentiation using calvarial osteoblasts and marrow stromal cells identifie

187 Ai mediated depletion of EMILIN-1 in primary calvarial osteoblasts and MC3T3-E1 cells only fibulin-4

188 OC expression in calvarial osteoblasts and odontoblasts is regulated in p

189 eletogenic mesenchyme, and, subsequently, to calvarial osteoblasts and osteoprogenitors.

190 ulation of Runx2 is also observed in primary calvarial osteoblasts and other osteoblastic cells with

191 uppression (luciferase reporter) in MC3T3-E1 calvarial osteoblasts as an assay.

192 wed increased mineral deposition by Enpp1-/- calvarial osteoblasts but decreased mineral deposition b

193 Using calvarial osteoblasts derived from wild-type and MN1 kno

194 ginning at the mineralization stage shown in calvarial osteoblasts ex vivo and supported by significa

195 Cultured RB1(-/-) calvarial osteoblasts fail to cease proliferation upon r

196 In calvarial osteoblasts from Col-luc transgenic mice carry

197 Calvarial osteoblasts from mice carrying floxed IGF-1R a

198 Calvarial osteoblasts from mice homozygous for the floxe

199 nd transcriptional activity were elevated in calvarial osteoblasts from TgMek-sp mice and reduced in

200 on in cocultures of spleen cells and primary calvarial osteoblasts from wild-type (WT) and IL-1R type

201 on of Runx2 to bone cell proliferation using calvarial osteoblasts from wild-type and Runx2-deficient

202 nthetic collagen peptide analog and cultured calvarial osteoblasts in conjunction with mass spectrome

203 gulates the expression of the OC promoter in calvarial osteoblasts in part by de-repression, antagoni

204 Sox2 is expressed in calvarial osteoblasts in vivo and we show that constitut

205 Expression of OST-PTP mRNA in primary rat calvarial osteoblasts is temporally regulated, and peak

206 Release of ATP in the primary calvarial osteoblasts occurred within 1 min of onset of

207 Calvarial osteoblasts prepared from c-Abl null mice show

208 Primary calvarial osteoblasts proliferated more quickly but had

209 Further, transplantation of primary rat calvarial osteoblasts revealed statistically significant

210 ling in TgFGF mice also induced apoptosis in calvarial osteoblasts that was not, however, corrected b

211 and analysis of differentiating primary rat calvarial osteoblasts verified that both IL-18 mRNA and

212 Treatment of fetal rat calvarial osteoblasts with a 70-kDa N-terminal fibronect

213 C3TC-E1 and RAW 264.7 cells), primary murine calvarial osteoblasts, and bone marrow-derived osteoclas

214 In MC3T3E1 calvarial osteoblasts, fibroblast growth factor receptor

215 To delete Cnb1 in vitro, primary calvarial osteoblasts, harvested from Cnb1(f/f) mice, we

216 Primary calvarial osteoblasts, isolated from 3-day-old NZO and c

217 both primary rat calvarial and MC3T3E1 mouse calvarial osteoblasts, transient expression of Dlx5 only

218 5 and Msx2 are both expressed by primary rat calvarial osteoblasts, we examined whether Msx2 and Dlx5

219 g the appropriate maturation and function of calvarial osteoblasts.

220 is shows that EN1 regulates FGF signaling in calvarial osteoblasts.

221 th plate chondrocytes, as well as in primary calvarial osteoblasts.

222 ense orientations, on primary cultured chick calvarial osteoblasts.

223 regulated during differentiation of MC3T3E1 calvarial osteoblasts.

224 RAP74 that regulate OC promoter activity in calvarial osteoblasts.

225 expression by FGF and cyclic AMP in MC3T3-E1 calvarial osteoblasts.

226 ed reduced N-cadherin expression in RB1(-/-) calvarial osteoblasts.

227 and it showed no effect on OPG expression in calvarial osteoblasts.

228 of Igfbp2(-/-) bone marrow stromal cells and calvarial osteoblasts.

229 Moreover, EN1 indirectly influences calvarial osteoclast recruitment and bone resorption by

230 s required for both early and late phases of calvarial osteogenesis.

231 s provides insight into normal mechanisms of calvarial osteogenesis.

232 Rat calvarial osteogenic cells were cultured on Ti disks wit

233 actor receptor 2 (Fgfr2) in regulating early calvarial osteogenic differentiation, and postulate that

234 n of activity in an MSX2-mediated pathway of calvarial osteogenic differentiation.

235 nium particle-induced osteoclastogenesis and calvarial osteolysis in vitro, ex vivo and in vivo.

236 ing/closed sutures in these animals revealed calvarial overgrowth and overlap along with increased os

237 In summary, Nell-1 overexpression induced calvarial overgrowth resulting in premature suture closu

238 Increased calvarial periosteal and tibial/femoral endosteal bone d

239 onses in affected (ie, where the head hurts) calvarial periosteum of (1) patients whose CMs are assoc

240 stitial collagenase mRNA was detected in the calvarial periosteum of PTH-treated, but not vehicle-tre

241 roinflammatory genes (eg, CCL8, TLR2) in the calvarial periosteum significantly increased in CM patie

242 the brain, fibrous sutures form between the calvarial plates.

243 over, elevated osteoclasts and intracortical/calvarial porosity is exacerbated by overexpressing Sost

244 Calvarial pre-osteoblasts from Bmpr1b mutant showed comp

245 Different from calvarial pre-osteoblasts, Bmpr1b mutant bone marrow mes

246 However when calvarial progenitor cells derived from the same transge

247 only by P. gingivalis LPS and FimA in mouse calvarial scalp, further confirming the differences of c

248 ved cells (ADCs) to regenerate critical size calvarial (superior portion of the skull) defects in mic

249 Calcein labeling of calvarial surfaces was increased in Col1a1(r/r) relative

250 actyly syndrome in which premature fusion of calvarial suture (craniosynostosis) is an infrequent but

251 efect model ex vivo as well as its effect on calvarial suture closure.

252 That it may function in calvarial suture development and figure in the pathophys

253 suggest a novel role for Gli3 in regulating calvarial suture development by controlling canonical Bm

254 s that infiltrate the periosteum through the calvarial sutures may be positioned to mediate migraine

255 expressed during premature bone formation in calvarial sutures of craniosynostosis patients.

256 e-specific overexpression of Msx2 within the calvarial sutures to address the developmental mechanism

257 icantly increase premature bone formation in calvarial sutures.

258 Axin2 to prevent the untimely closure of the calvarial sutures.

259 regulated chemokines CCL3 and CCL4 in murine calvarial tissue.

260 tivation of p38 signaling in mutant skin and calvarial tissues.

261 In addition, calvarial uptake correlated linearly with the number of

262 PTH treatment increased calvarial uptake of 64Cu-CB-TE2A-c(RGDyK), compared with

263 aB ligand (RANKL) or PTHrP in vivo increased calvarial vessel density and osteoclast number.