ライフサイエンスコーパス: hypertrophic chondrocyte

1 accelerated differentiation into postmitotic hypertrophic chondrocytes.

2 osteoblasts as well as in proliferating and hypertrophic chondrocytes.

3 dramatically suppresses Runx2 mRNA levels in hypertrophic chondrocytes.

4 of an actin-binding gelsolin-like protein in hypertrophic chondrocytes.

5 e-9 (MMP-9) leads to an accumulation of late hypertrophic chondrocytes.

6 tiation of proliferating chondrocytes toward hypertrophic chondrocytes.

7 ue-specific expression of type X collagen to hypertrophic chondrocytes.

8 then further differentiate into postmitotic hypertrophic chondrocytes.

9 ect is negated by an interaction with SP3 in hypertrophic chondrocytes.

10 hondrocytes; however, it enhanced it in (pre)hypertrophic chondrocytes.

11 it destabilized the mRNA in prehypertrophic-hypertrophic chondrocytes.

12 tion centers and delayed removal of terminal hypertrophic chondrocytes.

13 ferating chondrocytes and attenuated in (pre)hypertrophic chondrocytes.

14 gradation caused by Mmp13 deficiency in late hypertrophic chondrocytes.

15 nail and Slug mRNAs were highly expressed in hypertrophic chondrocytes.

16 ntiation and influences the disappearance of hypertrophic chondrocytes.

17 he bone, and the other cellular component is hypertrophic chondrocytes.

18 onversion of proliferating chondrocytes into hypertrophic chondrocytes.

19 being from articular perichondrial cells and hypertrophic chondrocytes.

20 receding the transition of chondrocytes into hypertrophic chondrocytes.

21 pressed by osteoblasts and at a low level by hypertrophic chondrocytes.

22 uration from prehypertrophic chondrocytes to hypertrophic chondrocytes.

23 lar growth plates and a relative increase in hypertrophic chondrocytes.

24 in all chondrocytes of both genotypes except hypertrophic chondrocytes.

25 rophic zone and inhibits their maturation to hypertrophic chondrocytes.

26 onversion of proliferative chondrocytes into hypertrophic chondrocytes.

27 iferative to prehypertrophic chondrocytes to hypertrophic chondrocytes.

28 chondrocytes, and apoptosis was inhibited in hypertrophic chondrocytes.

29 and decreased numbers of prehypertrophic and hypertrophic chondrocytes.

30 o mediate the regulation of transcription in hypertrophic chondrocytes.

31 isolate cDNAs for genes upregulated in chick hypertrophic chondrocytes.

32 requires a critical mass of adjacent ectopic hypertrophic chondrocytes.

33 collagen synthesis in monolayer cultures of hypertrophic chondrocytes.

34 y expressed within prehypertrophic and early hypertrophic chondrocytes.

35 ates pro-osteoclastogenic FGFR1 signaling in hypertrophic chondrocytes.

36 bones in response to Vegfa secreted by (pre)hypertrophic chondrocytes.

37 itor cells to their terminal maturation into hypertrophic chondrocytes.

38 pd3 in mice results in an increase in mature hypertrophic chondrocytes.

39 on of Hh activity and an increased number of hypertrophic chondrocytes.

40 ative zone and differentiate proximally into hypertrophic chondrocytes.

41 esults in a decrease of CXCR4 mRNA levels in hypertrophic chondrocytes.

42 restricts high levels of Ccn2 expression to hypertrophic chondrocytes.

43 cells prior to terminal differentiation into hypertrophic chondrocytes.

44 is expressed in the bone marrow adjacent to hypertrophic chondrocytes.

45 tenuation in phospho-Erk immunoreactivity in hypertrophic chondrocytes.

46 ype II expression and lack of development of hypertrophic chondrocytes.

47 ons consistent with the observed increase in hypertrophic chondrocytes.

48 lso type X collagen, suggesting formation of hypertrophic chondrocytes.

49 y genes are expressed in prehypertrophic and hypertrophic chondrocytes.

50 gh there was no up-regulation of markers for hypertrophic chondrocytes, a TUNEL assay showed a marked

51 nt, since targeting TAP63alpha expression in hypertrophic chondrocytes accelerates endochondral ossif

52 minished and there was a notable increase of hypertrophic chondrocytes, accompanied by premature ossi

53 analysis, and overexpression of Dlx5 in non-hypertrophic chondrocytes activates the proximal Col10a1

54 aled that the growth plate contained smaller hypertrophic chondrocytes and a thickened hypercellular

55 gulating mitochondrial membrane potential in hypertrophic chondrocytes and growth plate maturation by

56 ere is a striking reduction in the number of hypertrophic chondrocytes and in the expression domains

57 xhibited expanded zones of proliferating and hypertrophic chondrocytes and increased chondrocyte prol

58 tissue growth factor is highly expressed in hypertrophic chondrocytes and is required for chondrogen

59 atially-dependent phenotypic overlap between hypertrophic chondrocytes and osteoblasts at the chondro

60 t and differentiation of progenitor cells to hypertrophic chondrocytes and osteoblasts.

61 transcription factor for genes expressed in hypertrophic chondrocytes and osteoblasts.

62 s of Cre-deleter strains to demonstrate that hypertrophic chondrocytes and osteocytes, both of which

63 ein-1 (DMP1) is a major synthetic product of hypertrophic chondrocytes and osteocytes.

64 e-induced ERK1/2 phosphorylation in cultured hypertrophic chondrocytes and perform essential, but par

65 nfluencing the osteogenic differentiation of hypertrophic chondrocytes and provided insight into the

66 ut decreased mineralization and apoptosis of hypertrophic chondrocytes and reduced osteoclast number

67 drocytes reactivated Ras-ERK1/2 signaling in hypertrophic chondrocytes and reversed the expansion of

68 at FGF18 is necessary for Vegf expression in hypertrophic chondrocytes and the perichondrium and is s

69 substrate of MMP-9, accumulates in the late hypertrophic chondrocytes and their surrounding extracel

70 e matrix protein synthesized by osteoblasts, hypertrophic chondrocytes, and ameloblasts as well as od

71 hypertrophic chondrocytes, size of terminal hypertrophic chondrocytes, and column density.

72 ransglutaminases (TGases) are upregulated in hypertrophic chondrocytes, and correlative evidence sugg

73 pecialized cells, also including osteocytes, hypertrophic chondrocytes, and odontoblasts.

74 glycan aggregates and normal organization of hypertrophic chondrocytes, and suggest that cartilage ma

75 lopment, whereas ablation of C-Raf decreases hypertrophic chondrocyte apoptosis and impairs vasculari

76 ole for this signaling pathway in regulating hypertrophic chondrocyte apoptosis in growing mice.

77 late abnormalities, associated with impaired hypertrophic chondrocyte apoptosis, are observed in huma

78 isoforms are required for phosphate-induced hypertrophic chondrocyte apoptosis, mice lacking all thr

79 Low circulating phosphate levels impair hypertrophic chondrocyte apoptosis, whereas treatment of

80 Erk1/2 (Mapk3/1) phosphorylation, leading to hypertrophic chondrocyte apoptosis.

81 phospho-Erk1/2 immunoreactivity and impaired hypertrophic chondrocyte apoptosis.

82 Hypophosphatemia causes rickets by impairing hypertrophic chondrocyte apoptosis.

83 ormed to identify factors that contribute to hypertrophic chondrocyte apoptosis.

84 Further, ectopic hypertrophic chondrocytes are associated with ectopic bo

85 When hypertrophic chondrocytes are transfected with a cDNA co

86 confirm that the molecule is upregulated in hypertrophic chondrocytes (as much as eightfold).

87 an initial decrease in the number of mature hypertrophic chondrocytes at E15.5 in c-maf-null tibiae,

88 becular bone, and an abnormal persistence of hypertrophic chondrocytes at embryonic day 16.5 (E16.5).

89 HMGB1 protein accumulated in the cytosol of hypertrophic chondrocytes at growth plates, and its extr

90 showed that NT2 mRNA is highly expressed by hypertrophic chondrocytes but is minimally expressed by

91 and that CRYBP1 mRNA was highly expressed by hypertrophic chondrocytes, but at very low levels by res

92 , MGP is expressed by proliferative and late hypertrophic chondrocytes, but not by the intervening ch

93 for replacement of terminally differentiated hypertrophic chondrocytes by bone.

94 Inhibition of p38 MAPK in hypertrophic chondrocytes by either PTH, SB303580, or bo

95 Treatment of hypertrophic chondrocytes by PTH or by p38 MAPK inhibito

96 These findings reveal that hypertrophic chondrocytes can qualitatively modulate the

97 Over-expression of adseverin in non-hypertrophic chondrocytes causes rearrangement of the ac

98 poptosis, suggesting a normal progression of hypertrophic chondrocyte cell fate.

99 -Raf is the predominant isoform expressed in hypertrophic chondrocytes, chondrocyte-specific c-Raf kn

100 ceptor activator of NF-kappaB ligand) in the hypertrophic chondrocytes close to the marrow space and

101 from the Col10-Cre compound mice showed that hypertrophic chondrocytes contributed to ~80% of bone ce

102 te of MMP-9 that acts downstream to regulate hypertrophic chondrocyte death and osteoclast recruitmen

103 Furthermore, osteoblast- and hypertrophic chondrocyte-derived VEGF stimulated recruit

104 Although hypertrophic chondrocytes develop normally, apoptosis, v

105 f Sox9 confirmed the requirement of Sox9 for hypertrophic chondrocyte development, and in vitro and e

106 During endochondral bone formation, hypertrophic chondrocytes die and the cartilage is repla

107 Igf1 null hypertrophic chondrocytes differentiate normally in term

108 ondrocytes into osteoblasts or by a specific hypertrophic chondrocyte differentiation ability of Cbfa

109 Panx3(-/-) embryos exhibited delays in hypertrophic chondrocyte differentiation and osteoblast

110 by an OGA inhibitor, was able to induce pre-hypertrophic chondrocyte differentiation both in vitro a

111 These results identify Cbfa1 as a hypertrophic chondrocyte differentiation factor and prov

112 liferation and for the normal progression of hypertrophic chondrocyte differentiation into bone in th

113 e length is decreased approximately 10%, and hypertrophic chondrocyte differentiation is perturbed.

114 family members are crucial regulators of the hypertrophic chondrocyte differentiation program.

115 ced chondrocyte proliferation, inhibition of hypertrophic chondrocyte differentiation, and a delay in

116 decreased chondrocyte proliferation, delayed hypertrophic chondrocyte differentiation, and endochondr

117 e mutant protein and subsequently disrupting hypertrophic chondrocyte differentiation.

118 educing the MCDS-associated abnormalities in hypertrophic chondrocyte differentiation.

119 elements, indicating that Cbfa1 may control hypertrophic chondrocyte differentiation.

120 tilage precursor proliferation and inhibited hypertrophic chondrocyte differentiation.

121 These hypertrophic chondrocytes down-regulate Type X collagen

122 1 ratio is higher in hypertrophic versus non-hypertrophic chondrocytes, due to the significant decrea

123 hypertrophic chondrocytes, and with FGFR1 in hypertrophic chondrocytes during endochondral ossificati

124 c-maf is expressed in hypertrophic chondrocytes during fetal development (E14.

125 pressed in FGFR-positive prehypertrophic and hypertrophic chondrocytes during growth plate endochondr

126 pe that is a compound of prehypertrophic and hypertrophic chondrocytes, exited from the cell cycle an

127 However, cultured hypertrophic chondrocytes from these mice did not exhibi

128 These results suggest that hypertrophic chondrocytes have a novel, tissue-specific

129 hile differentiation of chondroblasts to pre-hypertrophic chondrocytes (IHH expression) is normal up

130 levated and sustained SOX9 in SHP2-deficient hypertrophic chondrocytes impaired their differentiation

131 The enlarged zone of hypertrophic chondrocytes in A17DeltaCh mice resembles t

132 Emergence of hypertrophic chondrocytes in Day 8-10 embryo limbs was a

133 t -99 to -87) retards a protein specific for hypertrophic chondrocytes in electrophoretic mobility sh

134 es in its upper zones (UGP) and maturing and hypertrophic chondrocytes in its lower zones (LGP), but

135 ostoses patients was much lower than that in hypertrophic chondrocytes in normal human growth plates.

136 Cbfa1-deficient mice lack hypertrophic chondrocytes in some skeletal elements, ind

137 f Has2 protein decreased in nSMase2-positive hypertrophic chondrocytes in the bones of mouse embryos.

138 5beta (GADD45beta) prolonged the survival of hypertrophic chondrocytes in the developing mouse embryo

139 Hypertrophic chondrocytes in the epiphyseal growth plate

140 increased growth potential, and 4-fold more hypertrophic chondrocytes in the epiphyseal plate (P<0.0

141 the alpha1 integrin subunit was detected in hypertrophic chondrocytes in the growth plate and in a s

142 g because of its expression both in terminal hypertrophic chondrocytes in the growth plate and in ost

143 ltaCh) have a significantly expanded zone of hypertrophic chondrocytes in the growth plate and retard

144 es from a dramatic increase in the volume of hypertrophic chondrocytes in the growth plate as they un

145 04 is expressed in embryonic osteoblasts and hypertrophic chondrocytes in the growth plate as well as

146 TUNEL staining revealed more apoptotic hypertrophic chondrocytes in the growth plate of Col2-Op

147 Hypertrophic chondrocytes in the growth plate play a piv

148 vascular invasion, and formation of ectopic hypertrophic chondrocytes in the growth plate.

149 o has a role in regulating the transition to hypertrophic chondrocytes in the growth plate.

150 day 15, there is an expansion in the zone of hypertrophic chondrocytes in the growth plate.

151 Hypertrophic chondrocytes in the TZ activate expression

152 drive beta-galactosidase expression in lower hypertrophic chondrocytes in transgenic mice.

153 t LOXL2 is expressed by pre-hypertrophic and hypertrophic chondrocytes in vivo, and that LOXL2 expres

154 EGFR activity reduced beta-catenin amount in hypertrophic chondrocytes in vivo.

155 , we made use of cultures of chick embryonic hypertrophic chondrocytes in which mineralization was tr

156 Since the amount of TGF-beta activated by hypertrophic chondrocytes increased with mineral appeara

157 underexpression of MGP in proliferative and hypertrophic chondrocytes induced apoptosis.

158 r levamisole treatment of Ank-overexpressing hypertrophic chondrocytes inhibited APase expression and

159 Transdifferentiation of hypertrophic chondrocytes into bone-forming osteoblasts

160 The maturation of immature chondrocytes to hypertrophic chondrocytes is regulated by parathyroid ho

161 nduction of MEK1/2-ERK1/2 phosphorylation in hypertrophic chondrocytes is required for phosphate-medi

162 The RARgamma-rich type X collagen-expressing hypertrophic chondrocytes lay below metaphyseal prehyper

163 eased phospho-ERK1/2 immunoreactivity in the hypertrophic chondrocyte layer and impaired vascular inv

164 tal death and a significant expansion of the hypertrophic chondrocyte layer of the growth plate, acco

165 have demonstrated that expansion of the late hypertrophic chondrocyte layer, characteristic of ricket

166 ttermates largely due to an expansion of the hypertrophic chondrocyte layer.

167 Conversely, Matn3 overexpression in hypertrophic chondrocytes led to inhibition of Bmp-2-sti

168 piphyseal chondroblasts ectopically activate hypertrophic chondrocyte markers.

169 s in shortened skeletal elements and delayed hypertrophic chondrocyte maturation and bone formation.

170 ence of aggrecan, thereby inducing premature hypertrophic chondrocyte maturation, leading to the nano

171 ilage RNA showed a 5-10-fold decrease in the hypertrophic chondrocyte molecular markers VEGF, MMP13,

172 than forming a typical narrow zone, Ihh(-/-) hypertrophic chondrocytes occupied an elongated central

173 owever, VEGF (Vegfa) immunoreactivity in the hypertrophic chondrocytes of c-Raf(f/f);ColII-Cre(+) mic

174 ne, was detected both in prehypertrophic and hypertrophic chondrocytes of mouse embryo bone cartilage

175 abundantly expressed in bone, including the hypertrophic chondrocytes of the growth plate where cart

176 a disrupted hexagonal lattice network in the hypertrophic chondrocyte pericellular matrix in Tg growt

177 Collagenase-3 is normally expressed in hypertrophic chondrocytes, periosteal cells, and osteobl

178 This accumulation of hypertrophic chondrocytes persists and is still observed

179 discrepancy between the in vitro and in vivo hypertrophic chondrocyte phenotypes revealed normal chon

180 og (IHH), synthesized by prehypertrophic and hypertrophic chondrocytes, regulates the site of hypertr

181 n defects with incomplete differentiation of hypertrophic chondrocytes; renal medullary dysplasia; ad

182 pontin, markers of hypertrophic and terminal hypertrophic chondrocytes, respectively.

183 Transfection of a CXCR4 cDNA into pre-hypertrophic chondrocytes results in a dose-dependent in

184 initial in vivo characterization of condylar hypertrophic chondrocytes revealed modest numbers of apo

185 stromal cells, osteoblasts, osteocytes, and hypertrophic chondrocytes secrete a C-type lectin domain

186 ber of proliferative chondrocytes, number of hypertrophic chondrocytes, size of terminal hypertrophic

187 omain compared to TAP63alpha, using the same hypertrophic chondrocyte-specific Col10a1 control elemen

188 a (the longest P63 isoform) is driven by the hypertrophic chondrocyte-specific Col10a1 regulatory ele

189 ification due to altered RUNX2 regulation of hypertrophic chondrocyte-specific genes during chondrocy

190 sion of both endogenous collagen X and other hypertrophic chondrocyte-specific genes.

191 X) collagen gene (Col10a1) is the only known hypertrophic chondrocyte-specific molecular marker.

192 ndothelial cells does not affect the zone of hypertrophic chondrocytes, suggesting that the main role

193 e other hand, the same assays showed that in hypertrophic chondrocytes, TCF x LEF x beta-catenin comp

194 ulated because of ectopically differentiated hypertrophic chondrocytes that had lost PPR.

195 ition of proliferating and non-proliferating hypertrophic chondrocytes that is markedly more normal i

196 entiation block led to a severe reduction in hypertrophic chondrocytes that normally produce vascular

197 nsition from prehypertrophic chondrocytes to hypertrophic chondrocytes, thus defining a novel mechani

198 tigated in osteochondro-progenitor cells and hypertrophic chondrocytes to ascertain these mechanisms.

199 liferating immature chondrocytes into mature hypertrophic chondrocytes to become osteoblasts at the e

200 ucial local signals from prehypertrophic and hypertrophic chondrocytes to both chondrocytes and preos

201 or decades, it has been widely accepted that hypertrophic chondrocytes undergo apoptosis prior to end

202 chondral bone formation postulates that most hypertrophic chondrocytes undergo programmed cell death

203 ssing cells, predominantly proliferating and hypertrophic chondrocytes, using "Cre-loxP"-mediated gen

204 al role for phosphate-regulated apoptosis of hypertrophic chondrocytes via activation of the caspase-

205 maturation appeared normal, but the zone of hypertrophic chondrocytes was not transformed into metap

206 n collagen type X, specifically expressed by hypertrophic chondrocytes, was utilized to monitor the t

207 zed prominently in the nucleus in late stage hypertrophic chondrocytes where Mmp-13 mRNA was expresse

208 lated kinase (ERK) was detected primarily in hypertrophic chondrocytes, where C-raf is expressed, and

209 Sox9 protein outlives Sox9 RNA in upper hypertrophic chondrocytes, where it contributes with Mef

210 ta mRNA coincident with Runx2 protein in pre-hypertrophic chondrocytes, whereas GADD45beta protein wa

211 small, immature chondrocytes enlarge to form hypertrophic chondrocytes, which express collagen X.

212 The terminal hypertrophic chondrocytes, which form the scaffold on wh

213 Delta-1 is expressed specifically in the hypertrophic chondrocytes while Notch-2 is expressed in

214 receptor CXCR4 is predominantly expressed in hypertrophic chondrocytes, while its ligand, chemokine s

215 liferating to postmitotic prehypertrophic to hypertrophic chondrocytes, while mesenchymal cells immed

216 ochondral process, and prolonged presence of hypertrophic chondrocytes with delay of vascular invasio

217 Incubation of hypertrophic chondrocytes with PTH (1-34) induces an inh

218 ccompanied by expansion of proliferating and hypertrophic chondrocytes within the cartilaginous growt

219 although there are a modest expansion of the hypertrophic chondrocyte zone and a modest increase in t

220 ion event would alleviate the phenotype, the hypertrophic chondrocyte zone in the cKO condyles was co

221 At 1 mo of age, the condylar hypertrophic chondrocyte zone in the cKO-mice was > thre

222 d trabecular bone formation and expansion of hypertrophic chondrocyte zone.