ライフサイエンスコーパス: chondrocyte

1 the effects of F4 in IL-1beta-stimulated OA chondrocytes.

2 ynamics in the pericellular matrix of living chondrocytes.

3 ne expression is repressed by SIRT1 in human chondrocytes.

4 t) in effecting MMP13 transcription in human chondrocytes.

5 cytotoxicity against normal human articular chondrocytes.

6 , mechanoelectrical transduction pathways in chondrocytes.

7 creep, for three-dimensional (3D) culture of chondrocytes.

8 on RUNX2-driven MMP13 gene expression in OA chondrocytes.

9 ne its role in regulating gene expression in chondrocytes.

10 1-mediated MMP13 gene expression in human OA chondrocytes.

11 levels and RUNX2 gene expression in human OA chondrocytes.

12 OX9 rescued the differentiation of MSCs into chondrocytes.

13 of miRNAs in normal and osteoarthritis (OA) chondrocytes.

14 divide more slowly than underlying articular chondrocytes.

15 tional and post transcriptional levels in OA chondrocytes.

16 nding of the mechanisms of action of ELF3 in chondrocytes.

17 induction of multiple signalling pathways in chondrocytes.

18 ring catabolic and inflammatory responses in chondrocytes.

19 mal stem cells, osteoblasts, osteocytes, and chondrocytes.

20 and other catabolic marker expression in OA chondrocytes.

21 sequestered in SGs in IL-1beta-stimulated OA chondrocytes.

22 x metalloproteinases in both mouse and human chondrocytes.

23 the hyperglucidic-mediated dysregulation of chondrocytes.

24 ting that SAHA inhibits IL-6 signaling in OA chondrocytes.

25 nt of methods to direct vectors to articular chondrocytes.

26 fferentiate into osteocytes, adipocytes, and chondrocytes.

27 of interconnected cartilage matrix formed by chondrocytes.

28 toire of miRNAs and isomiRs in primary human chondrocytes.

29 by deep sequencing analysis of primary human chondrocytes.

30 rtilage de novo, entirely substituting fetal chondrocytes.

31 s to a blockage of the autophagy flux in LSD chondrocytes.

32 s are derived via direct transformation from chondrocytes.

33 e growth by regulating glucose metabolism in chondrocytes.

34 artly by regulating the abundance of SOX9 in chondrocytes.

35 , MMP-13 and ADAMTS-4 in IL-1beta-treated OA chondrocytes.

36 MiR-146b expression was up-regulated in OA chondrocytes.

37 no up-regulation of markers for hypertrophic chondrocytes, a TUNEL assay showed a marked increase in

38 RF-R1 and CRF-R2, in primary human articular chondrocytes (AC) and demonstrate its role as an autocri

39 nditional deletion of the Phd2 gene (cKO) in chondrocytes accelerated the transition of progenitors t

40 Therefore, we summarize that chondrocytes actively mitigate local joint inflammation,

41 ntiate down multiple cell lineages including chondrocytes, adipocytes, osteoblasts, and multiple neur

42 we show that both pathways are activated in chondrocytes after treatment with TGF-beta and that TGF-

43 h of bones occurs at the growth plates where chondrocytes align into columns that allow directional g

44 on of endogenous glucocorticoid signaling in chondrocytes also modulates the course and severity of a

45 In this study, we found defects in chondrocyte and osteoblast differentiation in Spop-null

46 Indian Hedgehog (Ihh) regulates chondrocyte and osteoblast differentiation through the G

47 Panx3 regulates both chondrocyte and osteoblast differentiation via the activ

48 ed open chromatin regions recapitulate known chondrocyte and skeletal biology, are enriched at height

49 hat have the characteristics of osteoblasts, chondrocytes and adipocytes.

50 cells exhibit progenitor activity for stable chondrocytes and are able to self-organize three-dimensi

51 strated the key contribution of growth plate chondrocytes and articular chondrocytes, not only for lo

52 aphy, showed that superficial cells generate chondrocytes and contribute to the growth and reshaping

53 as a result of aging or injury contain dead chondrocytes and damaged cartilage.

54 nsition into prehypertrophic and hypetrophic chondrocytes and finally into osteoblasts expressing Col

55 catabolic gene expression in human articular chondrocytes and is sufficient to attenuate MMP activiti

56 rked cell-to-cell heterogeneity amongst both chondrocytes and mesenchymal stem cells undergoing chond

57 To elucidate the interplay between chondrocytes and nanocapsules and their therapeutic effe

58 dent phenotypic overlap between hypertrophic chondrocytes and osteoblasts at the chondro-osseous bord

59 , postnatal Gli1(+) cells contribute to both chondrocytes and osteoblasts during bone fracture healin

60 rom the proliferation and differentiation of chondrocytes and osteoprogenitor cells.

61 1/2 phosphorylation in cultured hypertrophic chondrocytes and perform essential, but partially redund

62 e osteogenic differentiation of hypertrophic chondrocytes and provided insight into the pathogenesis

63 ts metabolite, fall after treatment of mouse chondrocytes and rat tibia explants with IL-1beta, an in

64 ssion and signaling of Fgfr3 in growth plate chondrocytes and suppression of chondrocyte proliferatio

65 levels of phosphorylated VEGFR2 in articular chondrocytes and synovial cells and reduce levels of pho

66 GF is associated with catabolic processes in chondrocytes and synovial cells.

67 that obesity enhances the cross-talk between chondrocytes and synovial fibroblasts via raised levels

68 lture, mutant disc cells differentiated into chondrocytes and synthesized cartilage matrix more robus

69 ence for dysregulation within the glycome of chondrocytes and the network of a family of adhesion/gro

70 was observed between RUNX2 mRNA levels in OA chondrocytes and the percentage methylation of the CpG s

71 d for postnatal differentiation of articular chondrocytes and the timely ossification of bones in joi

72 they physically interact in the cytoplasm of chondrocytes, and loss of FlnA enhances FlnB expression

73 issues through its secretion by osteoblasts, chondrocytes, and mesenchymal cells.

74 lls, also including osteocytes, hypertrophic chondrocytes, and odontoblasts.

75 eas ablation of C-Raf decreases hypertrophic chondrocyte apoptosis and impairs vascularization of the

76 atrix loss without proteoglycan replacement, chondrocyte apoptosis at day 5, synovitis present at day

77 required for phosphate-induced hypertrophic chondrocyte apoptosis, mice lacking all three Raf isofor

78 Chondrocyte apoptosis, synovitis, and ectopic calcificat

79 /1) phosphorylation, leading to hypertrophic chondrocyte apoptosis.

80 2 immunoreactivity and impaired hypertrophic chondrocyte apoptosis.

81 mia causes rickets by impairing hypertrophic chondrocyte apoptosis.

82 e lower jaw of adult zebrafish, we show that chondrocytes are crucial for generating thick bone durin

83 Senescent chondrocytes are found in cartilage tissue isolated from

84 ning how hypoxia affects lipid metabolism in chondrocytes are lacking.

85 t mechanical load and the resulting force on chondrocytes are necessary during active growth for prop

86 Chondrocytes are responsible for the formation of the sk

87 rogenitors to hypertrophic (differentiating) chondrocytes as revealed by reduced SZ thickness, and in

88 ated with the ectopic chondrogenic cells and chondrocytes, as indicated by phosphorylated Smad 1/5/8

89 the proximal MMP13 AP-1 motif in stimulated chondrocytes at time points that no longer supported bin

90 Endogenous glucocorticoid signaling in chondrocytes attenuates joint inflammation and damage.

91 production, indicating an important role in chondrocyte biology.

92 otifs of transcription factors with roles in chondrocyte biology.

93 lts define a regulatory mechanism that links chondrocyte BMAL1 to the maintenance and repair of carti

94 ting S-phase entry and cell proliferation of chondrocytes both in vitro and in vivo, at least in part

95 H promoted expression of markers of immature chondrocytes but inhibited chondrocyte hypertrophy while

96 ) mRNA is observed in IL-1beta-stimulated OA chondrocytes but the synthesis of protein found signific

97 specifically suppresses protein synthesis in chondrocytes, but not in any other cells of mesenchymal

98 ese changes were prevented in cultured human chondrocytes by adenoviral expression of catalase target

99 specifically deleted in Aggrecan-expressing chondrocytes by administering tamoxifen at 8-weeks of ag

100 We found that lysis of articular chondrocytes by PBMC or polyclonal NK cells was potentia

101 x3 regulates the terminal differentiation of chondrocytes by promoting vascular endothelial growth fa

102 l types encountered in vivo, including human chondrocytes (C28/I2), human hepatic epithelial cells (L

103 eta-catenin signaling, a pathway involved in chondrocyte catabolism and OA.

104 Here we show that Eed deficiency in chondrocytes causes severe kyphosis and a growth defect

105 ssive destruction of articular cartilage and chondrocyte cell death.

106 B-cell) and mesenchymal (osteoblast lineage, chondrocyte) cell types.

107 Chondrocytes challenged with IL-1beta, a cytokine involv

108 redominant isoform expressed in hypertrophic chondrocytes, chondrocyte-specific c-Raf knockout mice (

109 During jawbone regeneration, we find that chondrocytes co-express genes associated with osteoblast

110 f the knee was increased in mice with intact chondrocytes compared with animals whose chondrocytes ha

111 Chondrocytes constitutively expressed LLT1, a ligand of

112 findings suggest that inhibition of Runx2 in chondrocytes could at least partially rescue DMM-induced

113 LLT1 expression by chondrocytes could be upregulated by IL-1alpha and TNF.

114 equivalents formed from hydrogels containing chondrocytes could provide a solution for replacing dama

115 In this work we show that chondrocytes cultured in hypoxia and normoxia can be dif

116 ace chondrocytes in mice and determined that chondrocyte death did not lead to cartilage damage.

117 hondrocytes had been killed, suggesting that chondrocyte death does not drive cartilage damage in res

118 In this study, we examined whether chondrocyte death undermines cartilage integrity in agin

119 activity, and CRISPR/Cas9 targeting of human chondrocytes demonstrates that the region regulates CHSY

120 served the absence of lineage progression of chondrocyte-derived bone cells to form osteoblasts and o

121 ion from synovial fibroblasts was induced by chondrocyte-derived IL-6.

122 e formation in much of the mandibular ramus (chondrocyte-derived) with intramembranous bone formation

123 s bone formation of the mandibular body (non-chondrocyte-derived).

124 ption factor that plays an essential role in chondrocyte development by directing the expression of c

125 interplay between Sox9 and AP-1 in mammalian chondrocyte development.

126 Primary human chondrocytes did not show any adverse effects upon nanoc

127 esses, whereas suppression of ECM1 enhances, chondrocyte differentiation and hypertrophy in vitro and

128 Rapamycin promotes chondrocyte differentiation and restores these defects i

129 indings that PHD2 is a negative regulator of chondrocyte differentiation and that hypoxia signaling i

130 ein and subsequently disrupting hypertrophic chondrocyte differentiation.

131 CDS-associated abnormalities in hypertrophic chondrocyte differentiation.

132 ecific inhibitor of PHD2, promoted articular chondrocyte differentiation.

133 iferation, its inactivation is essential for chondrocyte differentiation.

134 study, we established a role for lncRNAs in chondrocyte differentiation.

135 f this method for detecting abnormalities in chondrocyte distribution in mice lacking lubricin (Prg4)

136 A- and B-Raf ablation in chondrocytes does not alter skeletal development, wherea

137 GF acts as a survival factor in growth plate chondrocytes during development but only up until a few

138 eny of superficial cells fully replace fetal chondrocytes during early postnatal life.

139 ich is in marked contrast to the behavior of chondrocytes during facial skeletal development.

140 in the intracellular inflammation cascade of chondrocytes during the progress of osteoarthritis.

141 ined with cartilage, comprised of individual chondrocytes embedded in a specialized extracellular mat

142 Chondrocytes experience a complex mechanical environment

143 Chondrocytes experimentally depleted of cell-associated

144 M and non-T2DM patients as well as in murine chondrocytes exposed to high glucose (HG).

145 , particularly in the nuclear fraction, than chondrocytes exposed to normal glucose (NG).

146 ifen indicated that the same Col2 expressing chondrocytes expressed prehypertrophic, hypertrophic, an

147 As a consequence, LSD chondrocytes fail to properly secrete collagens, the mai

148 tion were observed in HG+IL-1beta-stimulated chondrocytes from Nrf-2(-/-) mice than in chondrocytes f

149 However, cultured hypertrophic chondrocytes from these mice did not exhibit impairment

150 nalysis of primary cultures of TMJ articular chondrocytes from wild-type and Ddr2(slie/slie) mice sho

151 ed chondrocytes from Nrf-2(-/-) mice than in chondrocytes from wild-type mice.

152 Transgenic restoration of Mgp expression in chondrocytes fully corrected the craniofacial anomalies

153 ver, the specific role of Runx2 in articular chondrocyte function and in OA development in adult mice

154 ate gene expression, play important roles in chondrocyte function and in the development of osteoarth

155 beta superfamily are important regulators of chondrocyte function.

156 expression and highlights a novel method of chondrocyte gene regulation involving a lncRNA.

157 n Jun- and Sox9-bound regions throughout the chondrocyte genome, reflecting direct binding of each fa

158 Fractions were added to C28/I2 chondrocytes, grown in micromasses, ions with or without

159 complex 1 (mTORC1) activity is required for chondrocyte growth and proliferation, its inactivation i

160 act chondrocytes compared with animals whose chondrocytes had been killed, suggesting that chondrocyt

161 HG-exposed, IL-1beta-stimulated chondrocytes had lower Nrf-2 levels in vitro, particular

162 ed globally in human chondroblastomas and in chondrocytes harboring the same genetic mutation, due to

163 s characterized by cartilage destruction and chondrocytes have a central role in this process.

164 With age and inflammation chondrocytes have reduced capacity to synthesize and mai

165 tivated in osteoarthritis, where it promotes chondrocyte hypertrophy and cartilage matrix catabolism.

166 roteinase 13 (MMP13) is also associated with chondrocyte hypertrophy in adult articular cartilage, th

167 uces cell cycle arrest and thereby initiates chondrocyte hypertrophy via BMP/SMAD-mediated up-regulat

168 rkers of immature chondrocytes but inhibited chondrocyte hypertrophy while IHH promoted chondrocyte h

169 d chondrocyte hypertrophy while IHH promoted chondrocyte hypertrophy.

170 ncreased MDZ thickness, as well as increased chondrocyte hypertrophy.

171 lysis of Sox9 binding profiles in developing chondrocytes identified marked enrichment of an AP-1-lik

172 ustained SOX9 in SHP2-deficient hypertrophic chondrocytes impaired their differentiation to osteoblas

173 Chondrocytes in injured and diseased situations frequent

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

175 ts guanylyl cyclase activity in growth plate chondrocytes in living bone.

176 f diphtheria toxin to kill articular surface chondrocytes in mice and determined that chondrocyte dea

177 gen, we cultured 3D pellets of human primary chondrocytes in normoxia (20% oxygen) and hypoxia (2.5%

178 A composition of the miRISC in primary human chondrocytes in response to IL-1beta treatment.

179 livery of therapeutic agents to the resident chondrocytes in the avascular cartilage.

180 assay showed a marked increase in apoptotic chondrocytes in the calcified nasal septum.

181 ealed that Sox9 and Col2 expressing immature chondrocytes in the epiphysis transition into prehypertr

182 and loss of FlnA enhances FlnB expression of chondrocytes in the growth plate (and vice versa), sugge

183 Hypertrophic chondrocytes in the TZ activate expression of the plurip

184 e similar increases in cilia length in human chondrocytes in vitro and after administration of dietar

185 tochondrial pathway that is not specific for chondrocytes in vitro or joint tissues in vivo.

186 Differentiation of stem cells to chondrocytes in vitro usually results in a heterogeneous

187 Treatment of primary articular chondrocytes, in vitro, with IOX2, a specific inhibitor

188 was secreted and it bound to osteoarthritic chondrocytes inhibitable by cognate sugar.

189 Since chondrocyte injury and subsequent cell death are the ear

190 feration and migration, but plays no role in chondrocyte intercalation.

191 nstrated the direct cell transformation from chondrocytes into bone cells in postnatal bone growth.

192 emonstrate that the direct transformation of chondrocytes into bone cells is common in both long bone

193 Transdifferentiation of hypertrophic chondrocytes into bone-forming osteoblasts has been repo

194 ontrol the transit of proliferating immature chondrocytes into mature hypertrophic chondrocytes to be

195 hat the abnormal MMP13 gene expression in OA chondrocytes is controlled by changes in the DNA methyla

196 ogical process, in which Bmpr1a signaling in chondrocytes is necessary for the formation of a pool or

197 EK1/2-ERK1/2 phosphorylation in hypertrophic chondrocytes is required for phosphate-mediated apoptosi

198 emoval of the SnCs from in vitro cultures of chondrocytes isolated from patients with OA undergoing t

199 P1A with specific mAbs resulted in increased chondrocyte killing.

200 AMP to adenosine) develop spontaneous OA and chondrocytes lacking A2AR develop an 'OA phenotype' with

201 etrant to human OA cartilage, and persist in chondrocyte lacunae for at least 2 wk.

202 -ERK1/2 immunoreactivity in the hypertrophic chondrocyte layer and impaired vascular invasion.

203 a significant expansion of the hypertrophic chondrocyte layer of the growth plate, accompanied by de

204 o studies demonstrated that loss of c-Raf in chondrocytes leads to expansion of the hypertrophic laye

205 Articular cartilage injury can result in chondrocyte loss and diminishment of specialised extrace

206 faces and in cortical osteocytes, epiphyseal chondrocytes, marrow adipocytes and mesenchymal stem cel

207 lar matrix deposition; this in turn promotes chondrocyte-matrix adhesion and cell proliferation.

208 e and Ddr2(slie/slie) mice showed defects in chondrocyte maturation and mineralization in the absence

209 development, which involves proper timing of chondrocyte maturation and perichondrial cell differenti

210 Cartilage homeostasis, chondrocyte maturation, and terminal differentiation mar

211 2) is critical for bone formation as well as chondrocyte maturation.

212 ity and is required for joint patterning and chondrocyte maturation.

213 odel of endochondral ossification holds that chondrocytes mature to hypertrophy, undergo apoptosis an

214 ion channels are of functional importance in chondrocyte mechanotransduction; however, direct evidenc

215 tes promotes TMJ degenerative remodelling by chondrocyte-mediated pro-catabolic activities.

216 characterized the dynamic repertoire of the chondrocyte miRNome and miRISC-associated miRNome by dee

217 n of growth plate chondrocytes and articular chondrocytes, not only for long bone growth, but also fo

218 (Vegfa) immunoreactivity in the hypertrophic chondrocytes of c-Raf(f/f);ColII-Cre(+) mice was signifi

219 onsequence of disruption of the Phd2 gene in chondrocytes on the articular cartilage phenotype in mic

220 e, in which the Smpd3 gene is knocked out in chondrocytes only, recapitulate the fro/fro mouse cartil

221 Chondrocytes or cartilage can also be activated by treat

222 letion did not give rise to an activation of chondrocytes or cartilage.

223 ivo In addition, target transgene of ECM1 in chondrocytes or osteoblasts in mice leads to striking de

224 ed dental cells ( Col1a1-cKO) or deletion in chondrocytes, osteoblasts, and craniofacial mesenchyme (

225 bone and involves a dynamic interplay among chondrocytes, osteoblasts, and endothelial cells.

226 iate along diverse lineages into adipocytes, chondrocytes, osteoblasts, fibroblasts, and myofibroblas

227 ict cartilage matrix formation and alter the chondrocyte phenotype.

228 h live imaging, the results show that single chondrocyte precursors can generate both single-column a

229 ide new insights into the effects of LiCl on chondrocyte primary cilia and Hedgehog signaling and sho

230 ic lineage tracing experiments have revealed chondrocyte progenitors at the articular surface.

231 Superficial cells are self-renewing chondrocyte progenitors, which form the articular cartil

232 led mTORC1 activity is crucial to coordinate chondrocyte proliferation and differentiation partially

233 t proteoglycans are essential components for chondrocyte proliferation and differentiation.

234 ed bone growth was associated with increased chondrocyte proliferation and expansion of the different

235 e for H3K27 methylation in the regulation of chondrocyte proliferation and hypertrophy in the growth

236 tissue growth factor (CTGF/CCN2) stimulates chondrocyte proliferation and maturation.

237 vement alters limb proportions and regulates chondrocyte proliferation in only specific growth plates

238 kyphosis and a growth defect with decreased chondrocyte proliferation, accelerated hypertrophic diff

239 growth plate chondrocytes and suppression of chondrocyte proliferation.

240 t activation of alpha2A-adrenergic signal in chondrocytes promotes TMJ degenerative remodelling by ch

241 he KBD articular cartilage (average positive chondrocyte rate = 47.59 +/- 7.79%) compared to healthy

242 ealthy articular cartilage (average positive chondrocyte rate = 64.73 +/- 5.05%).

243 lage destruction; however, the mechanisms of chondrocyte recognition by NK cells remain poorly unders

244 A sequencing we identified a human articular chondrocyte repertoire of lncRNAs from normal hip cartil

245 To better understand the chondrocyte's behavior in response to oxygen, we culture

246 w that the combined loss of Ezh1 and Ezh2 in chondrocytes severely impairs skeletal growth in mice.

247 form expressed in hypertrophic chondrocytes, chondrocyte-specific c-Raf knockout mice (c-Raf(f/f);Col

248 They show that chondrocyte-specific deletion of BMAL1 leads to cartilag

249 IL-3 increases the expression of mouse chondrocyte-specific genes, Sox9 and collagen type IIa,

250 e development by directing the expression of chondrocyte-specific genes.

251 Our work sheds further light on chondrocyte-specific SOX9 expression and highlights a no

252 istinct mechanical stimuli to primary murine chondrocytes, stretch of the membrane and deflection of

253 urse of chondrogenesis and its expression in chondrocytes strictly depends on parathyroid hormone-rel

254 VEGF is also a chondrocyte survival factor during development and essen

255 ting Ucn1 acts through CRF-R1 when promoting chondrocyte survival.

256 this IL-6 inflammatory response, mediated by chondrocyte-synovial fibroblast cross-talk, was enhanced

257 that mark OA progression in isolated primary chondrocytes taken from paired intact versus degraded ar

258 Tamoxifen-inducible chondrocyte-targeted glucocorticoid receptor-knockout (c

259 factor induced by inflammatory cytokines in chondrocytes that increases gene expression of catabolic

260 ation and consequent activation of mTORC1 in chondrocytes, the cells devoted to bone elongation.

261 In mutant chondrocytes, the mutations led to low levels of IFT81 a

262 yet down-regulates the HIF-1alpha pathway in chondrocytes, thereby promoting the demise of these cell

263 pothyroid mice, thus providing evidence that chondrocyte to osteoblast transdifferentiation is TH-dep

264 mature chondrocytes into mature hypertrophic chondrocytes to become osteoblasts at the epiphysis.

265 ut the mechanisms controlling the ability of chondrocytes to form columns.

266 show that susceptibility of normal articular chondrocytes to lysis by NK cells is modulated by NKR-P1

267 ntribute to Sox9 action in the transition of chondrocytes to the hypertrophic program.

268 interest are lncRNAs upstream of the master chondrocyte transcription factor SOX9 locus.

269 However, recent data demonstrate that chondrocytes transdifferentiate to osteoblasts in the gr

270 ersely, MMP13 gene expression was reduced in chondrocytes transfected with SIRT1 siRNA or treated wit

271 OA chondrocytes treated with F4 in the presence of IL-1beta

272 Furthermore, articular chondrocytes treated with OA derived extracellular vesic

273 Chondrocyte treatment with IL-1alpha resulted in their i

274 However, loss of chondrocyte TRPV4 did not prevent OA development followi

275 siological oxygen levels (19-21%), culturing chondrocytes under hypoxic oxygen levels (</=8%) promote

276 and sequestration of COX-2 mRNAs in human OA chondrocytes under pathological conditions.

277 of c-Fos/AP-1 expression and activity in OA chondrocytes under pathological conditions.

278 formation postulates that most hypertrophic chondrocytes undergo programmed cell death prior to bone

279 f Hif-1alpha expression in primary articular chondrocytes using lentiviral vectors containing Hif-1al

280 predominantly proliferating and hypertrophic chondrocytes, using "Cre-loxP"-mediated gene excision.

281 g exudate displayed protective activities on chondrocytes, using multiple readouts: these effects wer

282 mesenchymal stem cell markers, and generate chondrocytes via both asymmetric and symmetric different

283 ism for TGF-beta-mediated gene regulation in chondrocytes via p38 and phosphorylation and stabilizati

284 tructure, proteoglycan or collagen contents, chondrocyte viability or RNA expression levels were dete

285 on of the actin cytoskeleton in growth plate chondrocytes was disrupted.

286 Cell-mediated cytotoxicity against chondrocytes was evaluated by means of 18-h (51)Cr-relea

287 and protein expression data in human primary chondrocytes, we identified consistent molecular players

288 atrix metalloproteinases (MMPs) and RANKL by chondrocytes were evaluated.

289 Human OA articular chondrocytes were examined for miR-146b expression.

290 osis, mice lacking all three Raf isoforms in chondrocytes were generated.

291 Chondrocytes were isolated from articular cartilage obta

292 Human cartilage tissues and chondrocytes were obtained at autopsy from normal knee j

293 Chondrocytes were stimulated by norepinephrine to invest

294 gly, these effects could not be detected for chondrocytes which were pretreated with the nanocapsules

295 time that SIRT1 represses MMP13 in human OA chondrocytes, which appears to be mediated, at least in

296 ression of MMP-13 was determined by treating chondrocytes with recombinant IL-6 or by IL6 knockdown u

297 AC6 or following treatment of fibroblasts or chondrocytes with small molecule inhibitors of HDAC6.

298 e conclude that mechanical load and force on chondrocytes within the growth plate regulate postnatal

299 obe accumulation and the number of apoptotic chondrocytes within the injured xiphoid cartilage, which

300 ctopic expression in primary human articular chondrocytes, Wnt7a inhibited IL-1beta-induced MMP and i