ライフサイエンスコーパス: chondrocyte

1 d H3K36me3) in both hMSCs and differentiated chondrocytes.

2 TIMP3 and CPEB3 are putative miR targets in chondrocytes.

3 ous membrane with large pores to accommodate chondrocytes.

4 ntains or enhances mitochondrial function in chondrocytes.

5 kin-1beta (IL-1beta)-treated human articular chondrocytes.

6 d cis-regulatory elements were identified in chondrocytes.

7 is dispensable for survival of growth plate chondrocytes.

8 es their biased differentiation into Sox9(+) chondrocytes.

9 in the spontaneous [Ca(2+)](i) signaling of chondrocytes.

10 TrkA signaling in calcification of articular chondrocytes.

11 ation of large, stable monoclonal columns of chondrocytes.

12 ly associated with the de-differentiation of chondrocytes.

13 and suppressed proliferation in growth plate chondrocytes.

14 ate the influence of MSCs on the activity of chondrocytes.

15 ing in dysfunction and death of growth plate chondrocytes.

16 ggesting their splice-specific regulation in chondrocytes.

17 itiation of spontaneous [Ca(2+)](i) peaks in chondrocytes.

18 , PP2A was evaluated in MT-COMP growth plate chondrocytes.

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

20 tional and post transcriptional levels in OA chondrocytes.

21 preventing catabolic responses in activated chondrocytes.

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

23 levels and RUNX2 gene expression in human OA chondrocytes.

24 the hyperglucidic-mediated dysregulation of chondrocytes.

25 of interconnected cartilage matrix formed by chondrocytes.

26 toire of miRNAs and isomiRs in primary human chondrocytes.

27 by deep sequencing analysis of primary human chondrocytes.

28 rtilage de novo, entirely substituting fetal chondrocytes.

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

30 olic responses of inflammation in stimulated chondrocytes.

31 osteoarthritic cartilage and osteoarthritic chondrocytes.

32 pressed in arteries' smooth muscle cells and chondrocytes.

33 of human mesenchymal stem cells (hMSCs) into chondrocytes.

34 , regulatory, reparative and prehypertrophic chondrocytes.

35 gs which were recapitulated in primary human chondrocytes.

36 highly in micromass than monolayer cultured chondrocytes.

37 eta, a critical pro-inflammatory mediator in chondrocytes.

38 ndent on correct functioning of growth plate chondrocytes(1).

39 profiling of 10,640 synoviocytes and 26,192 chondrocytes: 12 distinct synovial cell types and 7 dist

40 hibited the spontaneous calcium signaling in chondrocytes, a fundamental signaling event in chondrocy

41 nd function was determined in primary murine chondrocytes, a human chondrocytic cell line (T/C-28a2),

42 mesenchymal stem cells (MSCs) and articular chondrocytes (ACs) in PLL-loaded hydrogels.

43 s, show that the encapsulated MSCs stimulate chondrocyte activity within a gel co-culture, both in te

44 termediate state that generated osteoblasts, chondrocytes, adipocytes, and macrophages.

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

46 b, CD49c and CD166 compared to donor-matched chondrocytes after 14 days in monolayer culture.

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

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

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

50 ich can increase the catabolic activities of chondrocytes and damage cartilage.

51 ovel factors that reduce catabolic events in chondrocytes and enhances chondrogenic differentiation o

52 They were transfected into CH-8 articular chondrocytes and HEK293 cells.

53 e persist into adulthood, both in peripheral chondrocytes and in cells of the fibrous perichondrium t

54 sion pattern of periostin splice variants in chondrocytes and ligament progenitor cells.

55 ymal cells, which differentiate further into chondrocytes and mature osteocytes.

56 l-based approaches, primarily based on using chondrocytes and mesenchymal stem cells (MSCs), are emer

57 enhance the protective microenvironment for chondrocytes and mesenchymal stem cells during inflammat

58 important role in the de-differentiation of chondrocytes and OA.

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

60 ence that RPL13 is present at high levels in chondrocytes and osteoblasts in mouse growth plates.

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

62 e syndrome, is expressed in mesoderm-derived chondrocytes and plays an essential and specific role in

63 It stimulates catabolic events in articular chondrocytes and prevents chondrogenic precursor cells f

64 -seq results at the same stage in developing chondrocytes and Sertoli cells and determined SOX9 targe

65 (LPM) generates tracheal mesoderm containing chondrocytes and smooth muscle cells.

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

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

68 uces matrix-degrading proteases in articular chondrocytes and synoviocytes, stimulating articular car

69 prevents formation of a mixed population of chondrocytes and tenocytes, and instead results in ectop

70 pathway in IL-1beta induced inflammation in chondrocytes and the ability of AM-ADSC to inhibit Wnt/b

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

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

73 clusive to synoviocytes and not expressed by chondrocytes) and their presence in osteoarthritic synov

74 drocytic cell line (T/C-28a2), primary human chondrocytes, and a murine model of OA by transmission e

75 sphorylated in prehypertrophic, hypertrophic chondrocytes, and bone areas of the newborn growth plate

76 FAM134B is required for protein secretion in chondrocytes, and cartilage growth and bone mineralizati

77 ic and -inflammatory effects on tumor cells, chondrocytes, and fibroblast-like synoviocytes.

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

79 oward an injury site, supply osteoblasts and chondrocytes, and recover new periosteum.

80 ck, reduction of the inflammatory profile in chondrocytes, and restoration of youthful regenerative r

81 of IL-1beta-induced p65 activity attenuated chondrocyte apoptosis and maintained cartilage homeostas

82 , the mechanism by which HFD/obesity induces chondrocyte apoptosis is not clearly understood.

83 While chondrocyte apoptosis rates in articular and growth plat

84 ingly, GC-induced bone growth impairment and chondrocyte apoptosis was prevented in HN overexpressing

85 cell-derived tryptase induces inflammation, chondrocyte apoptosis, and cartilage breakdown.

86 osteoarthritis (OA)-like lesions, including chondrocyte apoptosis, in the knee joints.

87 re and composition associated with increased chondrocyte apoptosis, which were not as evident in the

88 mia causes rickets by impairing hypertrophic chondrocyte apoptosis.

89 ic force microscopy showed that hypertrophic chondrocytes are the least mechanically stiff cells with

90 Chondrocytes are usually considered as nonexcitable cell

91 ing the spontaneous [Ca(2+)](i) signaling of chondrocytes as a combination of deterministic and stoch

92 nes was revealed in ACL progenitor cells and chondrocytes as well as in ACL progenitor cells in which

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

94 Monolayer cultured primary bovine articular chondrocytes (BACs) were subjected to cyclic tensile str

95 Cell sorting was used to separate chondrocytes based on tdTomato fluorescence and p16-high

96 e implications of a snoRNA in osteoarthritis chondrocyte biology and investigated its role in the cho

97 targets showed high similarity of targets in chondrocytes, but not in Sertoli cells.

98 ove high expression of a betaGeo reporter in chondrocytes, but not in the hypertrophic zone.

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

100 In addition, this pathway is activated in chondrocytes by FGF signaling, a critical regulator of s

101 respiration affects the survival of hypoxic chondrocytes by, at least in part, increasing intracellu

102 d GNF-5837 resulted in a strong induction of chondrocyte calcification, and gene expression data sugg

103 This study proved that chondrocytes can exhibit robust spontaneous [Ca(2+)](i)

104 lying mechanisms of this process and whether chondrocytes can generate other derivatives remain uncle

105 wth factors were predicted to regulate the 7 chondrocyte cell phenotypes.

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

107 Similarity analysis between hMSC and chondrocyte chromatin states defined in this study with

108 studies have demonstrated that coculture of chondrocytes (CHs) with bone marrow-derived mesenchymal

109 ea) mirrors that of mammals, with developing chondrocytes co-expressing genes encoding the transcript

110 Chondrocytes constitutively expressed LLT1, a ligand of

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

112 and stimulated anabolic events in articular chondrocytes cultured in an inflammatory environment.

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

114 trated that HFD induces ER stress to promote chondrocyte death and subchondral bone thickening, which

115 prevents the extreme hypoxia and the massive chondrocyte death observed in growth plates lacking Hif1

116 Mice on HFD also showed higher percentage of chondrocyte death, lower chondrocyte numbers per cartila

117 Transfection of miR-3085-3p into chondrocytes decreases expression of COL2A1 and ACAN, bo

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

119 CRISPR-edited osteosarcoma cell line, and in chondrocytes derived from osteoarthritis patients.

120 how how clinically relevant and mature nasal chondrocyte-derived engineered cartilage can be assessed

121 Nasal chondrocyte-derived engineered cartilage has been demons

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

123 as a mechanical loading-inducible factor in chondrocytes, detected at high levels in middle and deep

124 mechanical demands of bipedalism by altering chondrocyte developmental programs.

125 BX1 is crucial for the normal progression of chondrocyte differentiation in the spheno-occipital sync

126 yte biology and investigated its role in the chondrocyte differentiation status, rRNA levels and prot

127 -regulates expression of genes essential for chondrocyte differentiation, including Sox9, Col2a1, and

128 ccelerated mineralization due to accelerated chondrocyte differentiation, which is associated with ec

129 tween different epigenetic mechanisms during chondrocyte differentiation.

130 hange associated with repression of terminal chondrocyte differentiation.

131 rpolarized to depolarized state during early chondrocyte differentiation.

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

133 ein and subsequently disrupting hypertrophic chondrocyte differentiation.

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

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

136 t and the differentiation of osteoblasts and chondrocytes during skeletal development.

137 molecule OA drugs and their combinations to chondrocytes, enabling OA treatment with a single inject

138 Luciferase reporter assays confirmed that chondrocyte enhancers characterized in this study exhibi

139 Chondrocyte enhancers were associated with chondrogenesi

140 the transcription factor SOX9 is enriched in chondrocyte enhancers.

141 Chondrocytes experience a complex mechanical environment

142 ses contribute to osteoarthritis (OA), where chondrocytes experience a phenotypic shift towards hyper

143 In contrast, NF-kappaB inhibition in chondrocytes failed to reverse the effect of T1D.

144 artilage that provide a continuous supply of chondrocytes for endochondral ossification(1).

145 In primary murine chondrocytes from A2AR(-/-) null mice, which develop spo

146 rocytes from OA cartilage can be detected in chondrocytes from DDH cartilage before histological mani

147 s (ADSCs) exert paracrine effects protecting chondrocytes from degenerative changes.

148 of avascular and vascular meniscal cells and chondrocytes from medial OA knee joints (n = 10).

149 We investigated whether cellular changes in chondrocytes from OA cartilage can be detected in chondr

150 Formation of chondrocytes from SCPs also occurred in zebrafish, indic

151 SOC has evolved to protect the hypertrophic chondrocytes from the high mechanical stress encountered

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

153 den and diminished mitophagy, as compared to chondrocytes from WT animals.

154 data suggest that miR-3085-3p has a role in chondrocyte function and could contribute to the process

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

156 ntially expressed genes with a known role in chondrocyte function and osteoarthritis.

157 as an entirely novel molecular mechanism of chondrocyte function contextually linked with TMJ-OA.

158 assess the relationship between CD44-ICD and chondrocyte gene expression.

159 riants enriched in non-coding sequences near chondrocyte genes, loci that likely became optimized dur

160 so resulted in decreased expression of these chondrocyte genes.

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

162 the calcification process of human articular chondrocytes (hACs).

163 ifferential expression analysis of mRNA from chondrocytes harvested from knees of rats with PTOA trea

164 ource of cells capable of differentiating to chondrocytes has potential for repairing damaged cartila

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

166 ome activity have been described to regulate chondrocyte homeostasis in osteoarthritis, ribosome biog

167 A2A receptor (A2AR) stimulation and altered chondrocyte homeostasis which contributes to the pathoge

168 ter ligament structure, cartilage health, or chondrocyte homeostasis.

169 e-driven extracellular matrix remodeling and chondrocyte hypertrophic differentiation in vitro, in a

170 hibiting the expression of genes involved in chondrocyte hypertrophy and osteogenesis.

171 ular densities may also modulate MSC-derived chondrocyte hypertrophy in vitro.

172 TIMP3 and CPEB3 are putative miR targets in chondrocytes Identification of mechanically regulated mi

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

174 be used in the 3rd generation of Autologous Chondrocyte Implantation (ACI) in order to heal the dama

175 induced specific IKKalpha knockout in adult chondrocytes in AcanCreER(T2/+); IKKalpha(f/f) mice trea

176 e displayed elevated numbers of hypertrophic chondrocytes in articular calcified cartilage.

177 argeted elimination of p16(INK4a)-expressing chondrocytes in cartilage explant culture.

178 rentially expressed genes of healthy in situ chondrocytes in response to IL-1beta attack, which repre

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

180 Chondrocytes in situ from both groups show: (i) thicker

181 llae, which were present around hypertrophic chondrocytes in the ACC are described for the first time

182 entric lamellae, were identified surrounding chondrocytes in the ACC.

183 KMT2D mutant chondrocytes in the cranial base fail to properly differ

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

185 D271+ MSCs formed osteoblasts, adipocytes or chondrocytes in vitro.

186 ilage dense extracellular matrix renders the chondrocytes inaccessible, even to intra-articular injec

187 h cells staining for markers of hypertrophic chondrocytes, including collagen X and runt-related tran

188 silencing of HS6ST1 expression in primary OA chondrocytes inhibited extracellular signal-regulated ki

189 nt growth plate remodeling and conversion of chondrocytes into osteoblasts and marrow adipocytes as c

190 tudies support the direct differentiation of chondrocytes into osteoblasts and osteocytes in the TMJ.

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

192 colocalization of tissue strains to specific chondrocyte lacunar organizations within intact loaded j

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

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

195 show that prolonged HIF-1alpha signalling in chondrocytes leads to skeletal dysplasia by interfering

196 rly events in DDH cartilage originate at the chondrocyte level and that DDH cartilage may provide a n

197 on of the annulus fibrosus in the dKOs, with chondrocyte-like cells and fusion of dorsal processes.

198 vates the differentiation of prehypertrophic chondrocyte-like cells and inactivates Wnt signaling, bu

199 induced iPSC (CI-iPSC) constructs contained chondrocyte-like cells with abundant ECM components.

200 progenitors and attenuating the expansion of chondrocyte-like cells.

201 d to a Myh11(-), Lgals3(+) population with a chondrocyte-like gene signature that was markedly reduce

202 of ESCs to closely associated osteoblast or chondrocyte lineages.

203 e mitochondrial respiratory complex in human chondrocyte lines.

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

205 tensity of [Ca(2+)](i) peaks from individual chondrocytes maintain a consistent spatiotemporal patter

206 ing were examined in human healthy articular chondrocytes maintained under conditions supportive of o

207 Growth plate chondrocytes marked by sox10 and col2a1a contribute to o

208 n elevated the transcription of hypertrophic chondrocyte marker MMP13 and pre-osterix transcription f

209 the proportion of modulated SMCs expressing chondrocyte markers such as Col2a1 and Alpl, which local

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

211 ings reveal that TBX1 acts as a regulator of chondrocyte maturation and osteogenesis during the sphen

212 rotease inhibitors are crucial regulators of chondrocyte maturation program, growth plate integrity,

213 ule of osteoblastogenesis and a regulator of chondrocyte maturation, and suppresses its transcription

214 Cartilage homeostasis, chondrocyte maturation, and terminal differentiation mar

215 l regulator of the inflammatory responses in chondrocytes, may potentially mitigate the progression o

216 ling in chondrocytes, which are critical for chondrocyte mechanobiology.

217 ondrocytes, a fundamental signaling event in chondrocyte metabolic activities.

218 ther regions of the growth plate and whether chondrocyte metabolism controls cell function.

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

220 The chondrocyte nature of Snorc expression was confirmed in

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

222 While chondrocyte numbers in the OA group was notably decrease

223 igher percentage of chondrocyte death, lower chondrocyte numbers per cartilage area, and thickening o

224 Human osteoarthritis cartilage contains chondrocytes (OAC) and mesenchymal stromal cells (OA-MSC

225 CD44 fragmentation is enhanced in chondrocytes of osteoarthritis (OA) patients.

226 hat the perturbed Golgi secretory pathway of chondrocytes of the epiphyseal growth zone leads to dysp

227 , which were not as evident in the articular chondrocytes of the same animals.

228 capable of differentiating into adipocytes, chondrocytes, or osteocytes.

229 n signal into a skeletal cell type with dual chondrocyte/osteoblast properties.

230 plate, which provides a continuous supply of chondrocytes over a prolonged period.

231 Osteoarthritis presents as a change in the chondrocyte phenotype and an imbalance between anabolic

232 cts of IKKalpha in chondrocytes that control chondrocyte phenotype and impact on cell survival, matri

233 U3 snoRNA expression resulted in changes in chondrocyte phenotype.

234 e associated DNA methylation levels with the chondrocyte phenotype.

235 synovial cell types and 7 distinct articular chondrocyte phenotypes from matched tissues.

236 signaling (72 genes) in chondrocytes, while chondrocyte phenotypic shift was observed with histology

237 monstrated that the porous materials promote chondrocyte production.

238 posed to inhibit skeletal size by repressing chondrocyte proliferation and differentiation.

239 ication characterized by transiently reduced chondrocyte proliferation in mice at the early postnatal

240 Thus, YAP/TAZ activity controls chondrocyte proliferation in vitro, possibly reflecting

241 egenerative response, but is dispensable for chondrocyte proliferation in vivo, and instead functions

242 GC-induced suppression of chondrocyte proliferation was also prevented by HN.

243 pecific knockout of Yap/Taz does not prevent chondrocyte proliferation, differentiation or skeletal g

244 itro, Yap/Taz double knockout impairs murine chondrocyte proliferation, whereas constitutively nuclea

245 study of how disease-relevant signals affect chondrocyte protein translation at the transcriptomic le

246 in ribosomal RNA maturation, is critical for chondrocyte protein translation capacity in osteoarthrit

247 At the edge of the hypertrophic zone, chondrocytes re-enter the cell cycle and express leptin

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

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

250 itiation of spontaneous [Ca(2+)](i) peaks in chondrocytes requires the presence of extracellular Ca(2

251 Primary human chondrocytes responded to Nsp in vitro.

252 lationship by epigenetically profiling joint chondrocytes, revealing ancient selection and recent con

253 reviously identified miR-3085 in humans as a chondrocyte-selective microRNA, however it could not be

254 Inflammation leads to chondrocyte senescence and cartilage degeneration, resul

255 ular administration of gremlin-1 antibody or chondrocyte-specific deletion of Gremlin-1 decelerates o

256 Rich in Cartilage) has been identified as a chondrocyte-specific gene in the mouse.

257 Altogether these data confirmed the chondrocyte-specific nature of Snorc and revealed depend

258 thy and diseased adult cartilage, identified chondrocyte-specific regions of hypomethylation and the

259 verexpressed TIMP3 or [-1A]TIMP3 driven by a chondrocyte-specific type II collagen promoter.

260 ibe a neomorphic seed region mutation in the chondrocyte-specific, super-enhancer-associated MIR140 g

261 oth in terms of maintaining the coherence of chondrocyte spheroids, leading to a larger quantity of C

262 Furthermore chondrocyte spheroids, seeded on top of gels that contai

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

264 nd 8 were highly expressed only in articular chondrocytes, suggesting their splice-specific regulatio

265 dal cells reminiscent of ACL fibroblasts and chondrocytes surrounded by an extracellular matrix rich

266 scription factor HIF-1alpha is necessary for chondrocyte survival by unidentified cell-intrinsic mech

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

268 n obviates the need for Hif1alpha to promote chondrocyte survival under hypoxia.

269 nsic, cell-autonomous effects of IKKalpha in chondrocytes that control chondrocyte phenotype and impa

270 In chondrocytes, the mutation causes widespread derepressio

271 In OA chondrocytes, there is diminished mitochondrial producti

272 ness of the pericellular matrix (PCM) around chondrocytes thereby decreasing catabolic signaling.

273 e lamellae were associated with hypertrophic chondrocytes throughout the ACC.Novel microanatomical st

274 iscovered increased vasculature and putative chondrocyte to osteoblast transformation dually marked b

275 egatively regulate the release of FGF-2 from chondrocytes to allow IHH expression.

276 analysis shows that miR-3085-3p functions in chondrocytes to induce IL-1-signaling, reduce TGFbeta1 s

277 ealed the high vulnerability of hypertrophic chondrocytes to mechanical stress and showed that SOC pr

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

279 wed that the repressive effect of TGFbeta on chondrocytes treated with a pro-inflammatory stimulus re

280 precursor cells than conditioned medium from chondrocytes treated with IL-1beta alone.

281 Furthermore, articular chondrocytes treated with OA derived extracellular vesic

282 e early genetic responses of healthy in situ chondrocytes under IL-1beta attack with a focus on cell

283 Here we show that chondrocytes under inflammatory conditions undergo a met

284 ndral bone ossification is that hypertrophic chondrocytes undergo apoptosis, while invading vasculatu

285 Chondrocytes undergo changes to their protein translatio

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

287 teoarthritis-like conditions were studied in chondrocytes using interleukin-1 and osteoarthritic syno

288 HMWHA inhibits catabolic events in articular chondrocytes via the inhibition of p38 mitogen-activated

289 m IL-1beta and P15-1-treated human articular chondrocytes was less inhibitory for chondrogenic differ

290 chymal stem cells (BMSCs) to osteoblasts and chondrocytes was reduced, and migration and adhesion of

291 ur understanding of epigenetic regulation in chondrocytes we characterised the DNA methylation change

292 isms of spontaneous [Ca(2+)](i) signaling in chondrocytes, which are critical for chondrocyte mechano

293 This expansion of Sox9(+) chondrocytes, which is concomitant with decreased Notch2

294 g the induction and elimination of senescent chondrocytes, which will support investigations of senol

295 nes) and Rho GTPases signaling (72 genes) in chondrocytes, while chondrocyte phenotypic shift was obs

296 as enriched for homeostatic and hypertrophic chondrocytes, while damaged cartilage was enriched for p

297 ed to solid nanoparticles, are taken up into chondrocytes within 24 h, cleared from the cells within

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

299 ineage tracing studies in mouse suggest that chondrocytes within these templates persist and become o

300 al to differentiate into either tenocytes or chondrocytes, yet the developmental mechanism that spati