ライフサイエンスコーパス: growth plate

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

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

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

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

5 ations in collagen fiber organization in the growth plate.

6 and extracellular matrix of disc tissue and growth plate.

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

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

9 ry effects on chondrogenesis directly at the growth plate.

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

11 he identification of ciliary function in the growth plate.

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

13 eration and increased differentiation in the growth plate.

14 immotile chondrocytic primary cilium in the growth plate.

15 hondrocyte differentiation in the epiphyseal growth plate.

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

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

18 ondrocytes, followed by disappearance of the growth plate.

19 apoptosis and impairs vascularization of the growth plate.

20 drocytes, prevented the disappearance of the growth plate.

21 f the differentiation compartment within the growth plate.

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

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

24 ect in cell proliferation of chondrocytes in growth plate.

25 expressed in proliferating cells within the growth plate.

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

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

28 her detectable abnormality of the VHL mutant growth plates.

29 in hypertrophic chondrocytes in normal human growth plates.

30 s most between rapidly and slowly elongating growth plates.

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

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

33 adaptive responses of chondrocytes in fetal growth plates.

34 esting and proliferating chondrocytes of the growth plates.

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

36 hypertrophy, two key features of functional growth plates.

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

38 s chondrocyte proliferation in only specific growth plates.

39 or proper chondrocyte functions in embryonic growth plates.

40 ormed epigenetic profiling of murine femoral growth plates.

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

42 ses also revealed more organized and thinner growth plates.

43 of rapamycin) pathway activity in individual growth plates.

44 h phenotype was detected in their developing growth plates.

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

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

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

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

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

50 Growth plate abnormalities, associated with impaired hyp

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

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

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

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

55 In normal growth plates, ALK5 protein was strongly expressed in pe

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

57 ignaling has important and distinct roles in growth plate and articular cartilage and that postnatal

58 ent and organization and for function of the growth plate and articular cartilage.

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

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

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

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

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

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

65 is the most strongly expressed RAR in mouse growth plate and its expression characterizes the prolif

66 y decreased chondrocyte proliferation in the growth plate and lower trabecular bone density.

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

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

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

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

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

72 n modulating Ihh signaling in the developing growth plate, and highlights the importance of carbohydr

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

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

75 Their growth plates are defective and, importantly, display a

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

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

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

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

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

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

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

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

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

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

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

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

88 break down the terminal transverse septum of growth plate cartilage and permit capillaries to bud int

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

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

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

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

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

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

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

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

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

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

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

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

101 eceptor CD36, identified here as a marker of growth plate chondrocyte hypertrophy, mediates chondrocy

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

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

104 ACH), a severe dwarfing condition that has a growth plate chondrocyte pathology.

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

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

107 aces longitudinal bone growth by controlling growth plate chondrocyte proliferation and differentiati

108 Accumulated COMP in growth plate chondrocytes activates endoplasmic reticulu

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

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

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

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

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

114 1 expression is up-regulated in Jansen mouse growth plate chondrocytes and that PTHR1 is required for

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

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

117 Growth plate chondrocytes are organized in columns along

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

119 5% matrix deformation) of embryonic chicken growth plate chondrocytes in 3-dimensional (3D) collagen

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

121 2 decreases its guanylyl cyclase activity in growth plate chondrocytes in living bone.

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

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

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

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

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

127 Growth plate chondrocytes undergo a coordinated process

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

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

130 ownregulated in PTHrP null mutant (PTHrP-/-) growth plate chondrocytes, and (iii) blockage of ADAMTS-

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

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

133 8a overexpression decreased proliferation in growth plate chondrocytes, likely through up-regulation

134 pressed in proliferative and prehypertrophic growth plate chondrocytes, suggesting an autonomous func

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

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

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

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

139 n hypertrophic and terminally differentiated growth plate chondrocytes.

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

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

142 its the proliferation and differentiation of growth plate chondrocytes.

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

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

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

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

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

148 In ALK5(CKO) growth plates, chondrocytes proliferated and differentia

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

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

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

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

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

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

155 er adolescents, potentially after epiphyseal growth plate closure.

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

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

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

159 The growth plate contains resting and proliferating chondroc

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

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

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

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

164 vestigated the role of TGF-beta signaling in growth plate development by creating mice with a conditi

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

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

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

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

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

170 sence of circulating IGF-I, GH action at the growth plate, directly and via locally generated IGF-I,

171 d to hypocellularity in articular cartilage, growth plate disorganization, and a severe reduction in

172 Tibial and femoral growth plates displayed an excessive number of apoptotic

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

174 Normal growth plate distribution of ECM proteins was observed i

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

176 g capillaries on the metaphyseal side of the growth plate during endochondral bone growth.

177 ic animal models, resulting in a progressive growth plate dysplasia.

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

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

180 trophic and hypertrophic chondrocytes during growth plate endochondral ossification.

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

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

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

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

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

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

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

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

189 lar, exert previously unappreciated roles in growth plate function and skeletal growth and regulate a

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

191 Since aggrecan is critical for growth plate function, its deficiency in RAR-mutant mice

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

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

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

195 nanomelic (nm) chick mutant E12 fully formed growth plate (GP) is devoid of matrix and exhibits marke

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

197 ALK5(CKO) growth plates had an abnormally thin perichondrial cell

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 f hypertrophic differentiation in the mutant growth plates, indicating that HA is necessary for the n

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

212 formation and differentiation, as well as in growth plate integrity during skeletal development.

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

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

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

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

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

218 Hypertrophy of chondrocytes in growth plates is significantly impaired.

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 development such that the condyle loses its growth-plate-like cellular organization and no disk is f

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

223 e development of this surgical technique for growth plate manipulation for the treatment of angular d

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

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

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

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

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

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

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

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

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

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

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

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

236 te recapitulated the findings of human PSACH growth plate morphology, including (1) retention of ECM

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 The growth plates of Has2-deficient skeletal elements are se

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

246 hondrium, and the primary spongiosa in fetal growth plates of mice and chickens.

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

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

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

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

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

252 secreted glycoprotein that is important for growth plate organization and function.

253 In contrast, dramatic changes in growth plate organization in TSP3/5/Col9 knockout mice r

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

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

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

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

258 t form in the central regions of Has2 mutant growth plates owing to a failure of hypertrophic differe

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

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

261 In contrast, the structure of the MT-COMP growth plate recapitulated the findings of human PSACH g

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

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

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

265 of chondrocytes in HIF-2alpha-knockout mouse growth plate showed an elevated autophagic response thro

266 The paralyzed growth plate showed disruptions to column organization,

267 and immunohistochemical analysis of bm limb growth plates showed diminished Indian hedgehog (Ihh) si

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

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

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

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

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

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

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

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

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

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

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

279 In Atf4(-/-) growth plate, the typical columnar structure of prolifer

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

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

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

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

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

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

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

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

288 bases were deformed, and their synchondrosis growth plates were disorganized.

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

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

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

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

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

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

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

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.