ライフサイエンスコーパス: growth plate

1 ect in cell proliferation of chondrocytes in growth plate.

2 expressed in proliferating cells within the growth plate.

3 IHH, PTCH1, and FGFR3 mRNA expression in the growth plate.

4 ts, 73% fewer osteoclasts, and a 17% thicker growth plate.

5 chondrocytes, and bone areas of the newborn growth plate.

6 bone, 22% fewer osteoblasts, and 10% thinner growth plate.

7 ival, and hypertrophy of chondrocytes in the growth plate.

8 get of rapamycin (mTOR) in the cartilaginous growth plate.

9 ted cell-cell interactions in the developing growth plate.

10 and extracellular matrix of disc tissue and growth plate.

11 hat SOC reduces mechanical stress within the growth plate.

12 t have not previously been implicated in the growth plate.

13 bition by acting directly at the long bones' growth plate.

14 ry effects on chondrogenesis directly at the growth plate.

15 both in the diaphysis of the bone and in the growth plate.

16 n by transient expansion of cartilage in the growth plate.

17 he identification of ciliary function in the growth plate.

18 (IGF-1) both systemically and locally in the growth plate.

19 eration and increased differentiation in the growth plate.

20 immotile chondrocytic primary cilium in the growth plate.

21 hondrocyte differentiation in the epiphyseal growth plate.

22 ttern in the chondro-osseous junction of the growth plate.

23 o-localizes with GADD45beta in the embryonic growth plate.

24 ondrocytes, followed by disappearance of the growth plate.

25 drocytes, prevented the disappearance of the growth plate.

26 he least mechanically stiff cells within the growth plate.

27 ations in collagen fiber organization in the growth plate.

28 apoptosis and impairs vascularization of the growth plate.

29 f the differentiation compartment within the growth plate.

30 ceptor and may also act independently in the growth plate.

31 in ACH is targeting agents to the avascular growth plate.

32 h phenotype was detected in their developing growth plates.

33 her detectable abnormality of the VHL mutant growth plates.

34 in hypertrophic chondrocytes in normal human growth plates.

35 s most between rapidly and slowly elongating growth plates.

36 th BMP and TGFbeta signaling in Smad7 mutant growth plates.

37 osis was not altered compared with wild type growth plates.

38 adaptive responses of chondrocytes in fetal growth plates.

39 esting and proliferating chondrocytes of the growth plates.

40 ession of both collagen X and MMP13 in their growth plates.

41 hypertrophy, two key features of functional growth plates.

42 are similar in both the fetal and postnatal growth plates.

43 or proper chondrocyte functions in embryonic growth plates.

44 ) results in milder joint defects and normal growth plates.

45 els in chondrocytes and osteoblasts in mouse growth plates.

46 s chondrocyte proliferation in only specific growth plates.

47 ormed epigenetic profiling of murine femoral growth plates.

48 of rapamycin) pathway activity in individual growth plates.

49 se they are expressed in and function in the growth plate, a cartilaginous structure that causes bone

50 s, but its subsequent roles in the cartilage growth plate, a highly specialized structure that drives

51 ggest that these effects are attributable to growth plate abnormalities and premature cranial suture

52 ionally weaker bones that do not result from growth plate abnormalities or osteoblast dysfunction.

53 erforation, posterior leukoencephalopathy or growth plate abnormalities were not observed.

54 Growth plate abnormalities, associated with impaired hyp

55 of the hypertrophic chondrocyte layer of the growth plate, accompanied by decreased cleaved caspase-9

56 or tyrosine kinase that negatively regulates growth plate activity and linear bone growth.

57 aggrecans with TIMP deficiency, we uncouple growth plate activity in axial and appendicular bones.

58 Regulated growth plate activity is essential for postnatal bone de

59 ized mice, an increase in bone formation and growth plate activity predominates, resulting in equaliz

60 types of chondrocytes: articular (AA) versus growth plate (AG) cartilage chondrocytes in adult rats,

61 activities of caspase-3 and caspase-9 in the growth plate, along with a decrease in phosphorylation o

62 Growth plate and articular cartilage constitute a single

63 veloped normally, and histologic sections of growth plate and articular cartilage revealed no signifi

64 essential roles for Sox5/6 in promoting both growth plate and articular chondrocyte differentiation.

65 on alone or associated with GH on growth and growth plate and bone structure of young Hyp (the XLH an

66 ecause of the positive synergistic effect on growth plate and bone structures.

67 horylation and corrects the abnormal femoral growth plate and calvaria in organ cultures from embryos

68 Here, we review the development of the growth plate and cranial synchondrosis and the regulatio

69 tes transdifferentiate to osteoblasts in the growth plate and during regeneration, yet the mechanism(

70 ronic inflammation, which ultimately, causes growth plate and epiphyseal dysplasia in mice.

71 or tubacin reduced FGFR3 accumulation in the growth plate and improved endochondral bone growth.

72 Absence of phosphate at the growth plate and mineralising bone surfaces due to inade

73 ded zone of hypertrophic chondrocytes in the growth plate and retarded growth of long bones.

74 act, are co-expressed in chondrocytes in the growth plate and share overlapping expression in the cel

75 cortical bone, but it failed in normalizing growth plate and trabecular bone structures.

76 n the prehypertrophic zone in the developing growth plate and was induced during the differentiation

77 alpha signalling in the other regions of the growth plate and whether chondrocyte metabolism controls

78 ances FlnB expression of chondrocytes in the growth plate (and vice versa), suggesting compensation.

79 ailed analyses of LOXL2 expression in normal growth plates, and LOXL2 expression and function in deve

80 ures, reduced bone mineral content, expanded growth plates, and severe osteomalacia, with highly incr

81 include all primary ossification centres and growth plates, and therefore include at least the verteb

82 pecially since height-relevant tissues (e.g. growth plates) are difficult to study.

83 Synchondroses, consisting of mirror-image growth plates, are critical for cranial base elongation

84 ses structural collapse of the cartilaginous growth plate as a result of impaired proliferation, dela

85 e volume of hypertrophic chondrocytes in the growth plate as they undergo terminal differentiation.

86 eads to the formation of enchondromas in the growth plates as early as 8 weeks of age.

87 hondrocyte disorganization in the epiphyseal growth plate associated with decreased proliferation and

88 ice develop hypocellular cores in the medial growth plates, associated with elevated HIF1alpha levels

89 he cartilaginous long bone anlagen and their growth plates become delimited by perichondrium with whi

90 In addition, the centre of the expanding growth plate becomes hypoxic, and local activation of th

91 liferating chondrocytes of the cartilaginous growth plate but also in chondrocytes that have exited t

92 hypertrophic and proliferative zones of the growth plate, but mineralization of skeletal elements is

93 dergo proteolytic cleavage in the bovine rib growth plate, but this was not explored further.

94 he process of premature disappearance of the growth plate by postnatal inactivation of the PPR in cho

95 tal glycolysis to postnatal RC activation in growth plate cartilage and explain why RC dysfunction ca

96 Growth plate cartilage contributes to the generation of

97 fied that miR-1 is specifically expressed in growth plate cartilage in addition to muscle tissue, but

98 bone were disorganized and thicker while the growth plate cartilage in cKO mice was disorganized and

99 Direct targeting of therapeutic agents to growth plate cartilage may enhance efficacy and minimize

100 In endochondral bones, the growth plate cartilage promotes bone elongation via regu

101 chondrocyte apoptosis rates in articular and growth plate cartilage were similar between groups, homo

102 evident in the hypertrophic zone of AnxA6-/- growth plate cartilage, although apoptosis was not alter

103 which initiate the mineralization process in growth plate cartilage, resulted in reduced alkaline pho

104 ntitative analyses of cell behaviours in the growth plate cartilage, the template for long bone forma

105 In the growth plate cartilage, this balance is achieved in part

106 ent component of the extracellular matrix in growth plate cartilage.

107 in resting, proliferating, and hypertrophic growth-plate cartilage and assembles into an extended ex

108 y that characterize the Atf4(-/-) developing growth plate cartilages.

109 ide, primarily through SEs, to implement the growth plate chondrocyte differentiation program.

110 In mice, Smad3 deficiency accelerates growth plate chondrocyte maturation and leads to an oste

111 nd cellular context of FGFR signaling during growth plate chondrocyte maturation require tight, regul

112 oncentrations of FGF21 may directly suppress growth plate chondrocyte proliferation and differentiati

113 n important PTHrP target gene that regulates growth plate chondrocyte proliferation and differentiati

114 Accumulated COMP in growth plate chondrocytes activates endoplasmic reticulu

115 ore, we demonstrated the key contribution of growth plate chondrocytes and articular chondrocytes, no

116 sed proliferation and beta-catenin levels in growth plate chondrocytes and expanded the proliferative

117 zone cells develop is distinct from adjacent growth plate chondrocytes and is characterized by downre

118 inhibits hypertrophic differentiation in the growth plate chondrocytes and reduces Hedgehog (Hh) sign

119 creased expression and signaling of Fgfr3 in growth plate chondrocytes and suppression of chondrocyte

120 1 expression is up-regulated in Jansen mouse growth plate chondrocytes and that PTHR1 is required for

121 ate and multistep differentiation program of growth plate chondrocytes and thereby illuminate our und

122 ation of osteoblasts was autonomous from the growth plate chondrocytes and was correlated with an inc

123 Growth plate chondrocytes are organized in columns along

124 find that VEGF acts as a survival factor in growth plate chondrocytes during development but only up

125 5% matrix deformation) of embryonic chicken growth plate chondrocytes in 3-dimensional (3D) collagen

126 The loss of Sox9 in growth plate chondrocytes in knee joint and in NP cells

127 2 decreases its guanylyl cyclase activity in growth plate chondrocytes in living bone.

128 We then cultured mouse growth plate chondrocytes in the presence of graded conc

129 Sox9 and beta-catenin levels and activity in growth plate chondrocytes is an important underlying mec

130 this hypothesis, we used primary epiphyseal growth plate chondrocytes isolated from newborn mice wit

131 Growth plate chondrocytes marked by sox10 and col2a1a co

132 A global reduction of miRNAs in growth plate chondrocytes results in defects in both pro

133 O mice, Smad1 activity was increased more in growth plate chondrocytes than in wild-type mice.

134 Growth plate chondrocytes undergo a coordinated process

135 e, organization of the actin cytoskeleton in growth plate chondrocytes was disrupted.

136 B p65 is a transcription factor expressed in growth plate chondrocytes where it facilitates chondroge

137 s highly dependent on correct functioning of growth plate chondrocytes(1).

138 hly expressed in resting and prehypertrophic growth plate chondrocytes, as well as in articular chond

139 In cultured growth plate chondrocytes, FGF21 stimulated LEPROT and L

140 8a overexpression decreased proliferation in growth plate chondrocytes, likely through up-regulation

141 odel for proliferating/early prehypertrophic growth plate chondrocytes, we uncover that SOX6 and SOX9

142 ssential for survival and differentiation of growth plate chondrocytes, whereas HIF-2alpha is not nec

143 l respiration is dispensable for survival of growth plate chondrocytes.

144 nsated ER stress were detected in the mutant growth plate chondrocytes.

145 miR-140, causes a differentiation defect in growth plate chondrocytes.

146 Lin28a) to inhibit let-7 miRNA biogenesis in growth plate chondrocytes.

147 n hypertrophic and terminally differentiated growth plate chondrocytes.

148 nd activation) in fetal and 3-week-old mouse growth plate chondrocytes.

149 ation of beta-catenin levels and activity in growth plate chondrocytes.

150 ed apoptosis and suppressed proliferation in growth plate chondrocytes.

151 its the proliferation and differentiation of growth plate chondrocytes.

152 r signaling molecules are activated by GH in growth plate chondrocytes.

153 tress, resulting in dysfunction and death of growth plate chondrocytes.

154 tor of mTORC1, PP2A was evaluated in MT-COMP growth plate chondrocytes.

155 Loss of growth-plate chondrocytes by necroptosis was also found

156 In ACH human growth-plate chondrocytes, we demonstrated a decrease in

157 f mutant COMP protein and premature death of growth-plate chondrocytes.

158 Growth hormone (GH) stimulates growth plate chondrogenesis and longitudinal bone growth

159 ge number of novel genes that regulate human growth plate chondrogenesis and thereby contribute to th

160 In light of the inhibitory effects on growth plate chondrogenesis mediated by other FGFs, we h

161 lation of metatarsal longitudinal growth and growth plate chondrogenesis was neutralized by PDTC.

162 is an inducer of chondrocyte hypertrophy and growth plate chondrogenesis, although the specific molec

163 Both of the principal processes underlying growth plate chondrogenesis, chondrocyte proliferation a

164 le-knockout mice lacking all four TIMPs have growth plate closure in long bones, precipitating limb s

165 er adolescents, potentially after epiphyseal growth plate closure.

166 elevated in the prehypertrophic zone of the growth plate, coinciding with the Ihh expression region

167 oliferation and differentiation in embryonic growth plates compared with control littermates.

168 analysis of the long bones revealed that the growth plate contained smaller hypertrophic chondrocytes

169 The growth plate contains resting and proliferating chondroc

170 the tibias and femurs, and correction of the growth-plate defect.

171 double conditional knockout mice also showed growth plate defects and an arrest in chondrocyte prolif

172 with open eyes, misshapen heart valves, and growth plate defects.

173 re necessary during active growth for proper growth plate development and limb length.

174 The severe defects in growth plate development caused by chondrocyte extracell

175 n paracrine cascades, which promote abnormal growth plate development in NOMID mice.

176 tion of the chondrocyte phenotype during the growth plate development via direct targeting of HDAC4.

177 hereas HIF-2alpha is not necessary for fetal growth plate development.

178 le delay of growth but instead uncoordinated growth plate development.

179 S1P ablation results in rapid growth plate disruption due to intracellular Col II entr

180 ired to mediate cell stress responses in the growth plate during development.

181 signaling is necessary to achieve harmonious growth plate elongation and structure.

182 ively active in the absence of ligand in the growth plate, enabling ICI to act as an inverse agonist.

183 trophic and hypertrophic chondrocytes during growth plate endochondral ossification.

184 ions originated from an area proximal to the growth plate, expressed osteogenic cell markers, and sho

185 ng of bone development within the epiphyseal growth plate, factors that regulate periosteal osteogene

186 n Sox5(-/-)6(-/-) growth plates suggest that growth plate failure contribute to this Sox5(-/-)6(-/-)

187 ries may represent ankle sprains rather than growth plate fractures.

188 gradually replaced by a fully functional new growth plate from progenitor stem cells capable of suppo

189 mice revealed that the hypertrophic zone of growth plates from newborn AnxA6-/- mice was reduced in

190 logical analysis of femoral, tibial, and rib growth plates from newborn mice revealed that the hypert

191 In control growth plates from unaffected persons, however, heparana

192 ned analysis strongly implicates 78 genes in growth plate function, including multiple genes that par

193 WAS loci that are likely required for normal growth plate function.

194 , particularly near differentially expressed growth plate genes, and enriched for binding motifs of t

195 ed chondrocytes isolated from rat metatarsal growth plates, GH induced NF-kappaB-DNA binding and chon

196 ilia-GFP mice, we found presence of cilia on growth plate (GP), cartilage endplate (EP) annulus fibro

197 In the long bones, the growth plates (GPs) drive elongation by generating a sca

198 mice induced a significant expansion in the growth plate height and in the hypertrophic zone height.

199 it reduced fat mass, thymus weight, and the growth plate height in wild-type but not in ERalphaAF-2(

200 d inverse agonistic activity was seen on the growth plate height, resulting in enhanced longitudinal

201 -beta signaling is a critical determinant of growth plate homeostasis, skeletal dysplasias are often

202 al dysplasias are caused by dysregulation of growth plate homeostasis.

203 sible role of PPR signaling in the postnatal growth plate; however, the role of PPR signaling in post

204 pression microarray studies of mouse and rat growth plate, human disease databases and a mouse knocko

205 reduced the MCDS-associated expansion of the growth plate hypertrophic zone, attenuated enhanced expr

206 SDF-1 infiltrates cartilage and accelerates growth plate hypertrophy.

207 y higher in hypertrophic than upper zones of growth plate; (ii) such difference likely reflects disti

208 spike" was observed in the mid-region of the growth plate in the long bones of all NOMID mice that ma

209 creased bone mass and notable changes in the growth plate, including increased BrdU incorporation and

210 confirmed SH1DF, and 2 of these were partial growth plate injuries.

211 egulators of chondrocyte maturation program, growth plate integrity, and skeletal proportionality.

212 plasias and often manifest as short stature, growth-plate irregularities, and vertebral anomalies, su

213 zone of the Gadd45beta(-/-) mouse embryonic growth plate is compressed, and expression of type X col

214 mad1/5(CKO) mutant mouse, whose disorganized growth plate is due to the conditional deletion of Smad

215 The primary growth plate is eradicated by apoptosis but is gradually

216 ggesting that the main role of ADAM17 in the growth plate is in chondrocytes.

217 Hypertrophy of chondrocytes in growth plates is significantly impaired.

218 nd the massive chondrocyte death observed in growth plates lacking Hif1a.

219 re severe reduction in body size, weight and growth plate length, than observed in mice following kno

220 vitro through sclerotome specification into growth plate-like chondrocytes, a mechanism resembling i

221 ive symphyseal joint site, and established a growth-plate-like structure with distinct Ihh, collagen

222 Hence, growth plate maturation and bone formation can be uncoup

223 Extracellular phosphate plays a key role in growth plate maturation by inducing Erk1/2 (Mapk3/1) pho

224 Thus, c-Raf plays an important role in growth plate maturation by regulating vascular invasion,

225 e potential in hypertrophic chondrocytes and growth plate maturation by the parathyroid hormone-relat

226 The deletion of Shn2 and Shn3 impairs growth plate maturation during endochondral ossification

227 R2, led to the rescue of joint formation and growth plate maturation in Tgfbr2(Prx1KO) but an acceler

228 nd Col II deposition and functions to couple growth plate maturation to trabecular bone development i

229 essential, but partially redundant roles in growth plate maturation.

230 equired for phosphate-mediated apoptosis and growth plate maturation.

231 were generated to define a role for c-Raf in growth plate maturation.

232 B-Raf (Braf) in chondrocytes does not alter growth plate maturation.

233 echanical architecture of cortical bone, the growth plate, metaphysis, and marrow in fresh murine bon

234 ion in Tgfbr2(Prx1KO) but an acceleration of growth plate mineralization in control mice.

235 oduced in cartilage, we detected BMP9 in the growth plate, most likely derived from the circulation.

236 inal bone growth in children is sustained by growth plates, narrow discs of cartilage that provide a

237 e apoptotic hypertrophic chondrocytes in the growth plate of Col2-Opg mice.

238 ntally observed chondrocytic arrangements in growth plate of each of the Smad1/5(CKO) and control mic

239 alcified cartilage in a large area below the growth plate of endochondral bones.

240 bcutaneously, was able to penetrate into the growth plate of Fgfr3Y367C/+ mice and modify its organiz

241 NA expression in the liver and in the tibial growth plate of wild-type (WT) mice was increased compar

242 ed chondrocytes were prominent in epiphyseal growth plates of bones in Spg20-/- mice, perhaps explain

243 ding MAPK, SOX9, STAT1, and PLCgamma, in the growth plates of Fgfr3Y367C/+ mice and in cultured chond

244 al articular cartilage damage, the postnatal growth plates of IKKalpha cKO mice after DMM displayed a

245 e results in severe cartilage defects in the growth plates of long bones.

246 cifically, we studied the alterations of the growth plates of mutant mice in which chondrocytes lacke

247 d the extracellular matrix was softer in the growth plates of newborn P4ha1(+/-);P4ha2(-/-) mice.

248 overexpression of ECM1 rescues disorganized growth plates of PTHrP-null mice.

249 wever, unlike early embryonic ablations, the growth plates of these mice exhibit a lack of Ihh, PTHrP

250 atment reduced Indian Hedgehog expression in growth plates of wild-type mice but not in HN overexpres

251 ion labelling studies to evaluate changes in growth plate organisation, and unbiased array profiling

252 ere used to assess the impact of aggrecan on growth plate organization, chondrocyte survival and prol

253 en IX ablation results in severely disturbed growth plate organization, hypocellular regions, and abn

254 for joint formation and contribute to proper growth plate organization.

255 rickets and, notably, almost normalized the growth plate organization.

256 loproteinase 9 (Mmp9) and Mmp13 and enhanced growth plate osteoclastogenesis, as well as increased se

257 nt biological pathways (e.g., bone/cartilage/growth plate pathways) than do loci with no effect on SH

258 ound chondrocytes in the resting zone of the growth plate provide precursors for columnar chondrocyte

259 regions, but strong in narrow articular and growth plate regions crucial for bone development.

260 al load and force on chondrocytes within the growth plate regulate postnatal development of the long

261 Our data support Mmp9-dependent growth plate remodeling and conversion of chondrocytes i

262 etalloproteinase 9 (mmp9) results in delayed growth plate remodeling and fewer marrow adipocytes.

263 ne marrow but also within the periosteum and growth plate reserve zone.

264 ion and differentiation programme within the growth plate, resulting in uncontrolled cell proliferati

265 The paralyzed growth plate showed disruptions to column organization,

266 s consistent with in vivo results from mouse growth plates showing that Hmgb2 is expressed in prolife

267 unohistochemistry to study the expression of growth plate-signaling molecules and molecules shown to

268 FlnA and FlnB interactions in the cartilage growth plate, since mutations in both molecules cause ch

269 aling disrupts chondrocyte proliferation and growth plate size and architecture, leading to various c

270 l tissue specificities in the digit anlagen, growth plates, skull sutures and fingertips.

271 retarded and had marked alterations in both growth plate structure and dynamics as well as defective

272 , increased cilia length, aberrant cartilage growth plate structure, defective Hedgehog and altered E

273 n and weak Ihh expression in Sox5(-/-)6(-/-) growth plates suggest that growth plate failure contribu

274 i1(+) cells residing immediately beneath the growth plate, termed here "metaphyseal mesenchymal proge

275 to increased TGF-beta/SMAD signaling in the growth plate that was associated with reduced chondrocyt

276 In the growth plate, the interplay between parathyroid hormone-

277 ound Kif22 to be strongly upregulated at the growth plate, the precise pathogenetic mechanisms remain

278 cholesterol levels and a higher frequency of growth plate thickening in comparison to Aip+/, Prkar1a+

279 , early hypertrophic transition, and reduced growth plate thickness.

280 ental roles in the preservation of postnatal growth plate through chondrocyte differentiation and Col

281 ells in the context of the three-dimensional growth plate tissue.

282 of interest are transferred from the 96-well growth plates to soil.

283 prenatally and did not negatively affect the growth plate until 3 weeks after birth.

284 In mildly affected mutants, the condylar growth plate was dysfunctional and exhibited thicker sup

285 y normal growth, and the morphology of their growth plates was correct.

286 Aggrecan-null growth plates were devoid of matrix and lacked chondrocy

287 two-thirds and lower one-third of rabbit rib growth plates were microsurgically isolated and processe

288 Longitudinal growth of bones occurs at the growth plates where chondrocytes align into columns that

289 drocyte proliferation and hypertrophy in the growth plate, which are the central determinants of skel

290 ignaling lowers cyclic GMP production in the growth plate, which counteracts bone elongation.

291 ation of long bones is primarily through the growth plate, which is a cartilaginous structure at the

292 We tested this hypothesis in the fetal growth plate, which is hypoxic.

293 chondrocytes in the avascular hypoxic fetal growth plate, which is rich in extracellular matrix (ECM

294 ration and maturation of chondrocytes in the growth plate, which is the 'engine' of bone elongation.

295 niche develops postnatally in the epiphyseal growth plate, which provides a continuous supply of chon

296 relevant epigenetic information (here, from growth plates) with genetic association results can iden

297 ly expressed in the hypertrophic zone of the growth plate, with an 8-fold increase compared with the

298 o expansion of the hypertrophic layer of the growth plate, with decreased phospho-Erk1/2 immunoreacti

299 ic analysis of knee joints revealed abnormal growth plates, with loss of chondrocytes and growth arre

300 n cartilage induced lateral outgrowth of the growth plate within 2 weeks after ablation.