ライフサイエンスコーパス: articular chondrocyte

1 le of NGF-TrkA signaling in calcification of articular chondrocytes.

2 ic protein 1 (OP-1) signaling in adult human articular chondrocytes.

3 ting in long-term induction of IL1B in human articular chondrocytes.

4 sis factor alpha-induced cell death in human articular chondrocytes.

5 ical role in the development and function of articular chondrocytes.

6 ttermates and in primary chicken and porcine articular chondrocytes.

7 mbers and activins than are superficial zone articular chondrocytes.

8 onal activator of of MMP-13 by bFGF in human articular chondrocytes.

9 ynovial lining, subsynovial vasculature, and articular chondrocytes.

10 ory cytokines or by fibronectin fragments in articular chondrocytes.

11 pendent stimulation of MMP-13 in human adult articular chondrocytes.

12 beta)-induced NF-kappaB signaling cascade in articular chondrocytes.

13 enhances cartilage matrix synthesis by human articular chondrocytes.

14 d transfection of primary and passaged human articular chondrocytes.

15 igated MMP-13 production by bFGF using human articular chondrocytes.

16 A from SW1353 chondrocytes and primary human articular chondrocytes.

17 thin intron 1 of the gene expressed by human articular chondrocytes.

18 s show changes in the pericellular matrix of articular chondrocytes.

19 udied in transfected human immortalized CH-8 articular chondrocytes.

20 IMPs were found in IL-1+OSM-stimulated human articular chondrocytes.

21 inflammation and altered differentiation of articular chondrocytes.

22 However, RANKL does not activate human articular chondrocytes.

23 uced nitric oxide (NO) production from human articular chondrocytes.

24 APK mediate FN-f induced activation of human articular chondrocytes.

25 -alpha-induced NO production in normal human articular chondrocytes.

26 l-mediated cytotoxicity against normal human articular chondrocytes.

27 (inner ear hair cells and Merkel cells) and articular chondrocytes.

28 hritis was similar to that in cultured human articular chondrocytes.

29 le in matrix assembly and retention by human articular chondrocytes.

30 marily responsible for HA synthesis in human articular chondrocytes.

31 ssion of IL-18 and its role in regulating in articular chondrocytes.

32 thritis (OA), we studied PTHrP expression by articular chondrocytes.

33 1 and 2 stimulate the metabolic activity of articular chondrocytes.

34 lar results were obtained in fetal and adult articular chondrocytes.

35 E) in interleukin (IL)-1 activation of human articular chondrocytes.

36 ecently been demonstrated to be expressed in articular chondrocytes.

37 tibody to PTHrP increased PPi elaboration by articular chondrocytes.

38 i accumulation versus proliferation in human articular chondrocytes.

39 the spherical configuration of primary human articular chondrocytes.

40 ial cells divide more slowly than underlying articular chondrocytes.

41 development of methods to direct vectors to articular chondrocytes.

42 le of autophagy in ACV production by primary articular chondrocytes.

43 on of Prg4, specifically in superficial zone articular chondrocytes.

44 V4 transduces dynamic compressive loading in articular chondrocytes.

45 the cartilage, and enhanced proliferation of articular chondrocytes.

46 n interleukin-1beta (IL-1beta)-treated human articular chondrocytes.

47 hic growth plate chondrocytes, as well as in articular chondrocytes.

48 ction by LfcinB-ERK-AP-1 axis in human adult articular chondrocytes.

49 le of TCF/LEF transcription factors in human articular chondrocytes.

50 flammatory and chondroprotective cytokine in articular chondrocytes.

51 DOT1L is also expressed in OA articular chondrocytes.

52 ct regulator of SOX9 in normal healthy human articular chondrocytes.

53 ation in surface zone cartilage and isolated articular chondrocytes.

54 expression was detected in rodent and human articular chondrocytes.

55 matrix-degrading enzyme production in human articular chondrocytes.

56 growth chondrocytes and is also expressed in articular chondrocytes.

57 ubtypes, CRF-R1 and CRF-R2, in primary human articular chondrocytes (AC) and demonstrate its role as

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

59 arkers by which to distinguish NP cells from articular chondrocytes (ACs).

60 Nitric oxide (NO) is generated copiously by articular chondrocytes activated by interleukin-1beta (I

61 Human articular chondrocytes actively produce reactive oxygen

62 ation of both DDR-2 and MMP-13 mRNA in human articular chondrocytes after stimulation with type II co

63 n rat chondrosarcoma cells and primary human articular chondrocytes after treatment with TNFalpha was

64 Articular chondrocyte and cartilage cultures were stimul

65 s was used to identify clonal cell lines for articular chondrocyte and hypertrophic chondrocyte proge

66 ng osteogenic plasticity of growth-plate and articular chondrocytes and a SOX9-countered chondrocyte

67 primary cells with known TRPV4 expression - articular chondrocytes and astrocytes.

68 ndrocytes and cartilage, but decreased in OA articular chondrocytes and cartilage and in normal chond

69 n status of AMPKalpha Thr(172) in human knee articular chondrocytes and cartilage by Western blotting

70 Human articular chondrocytes and cartilage explants (obtained

71 Human articular chondrocytes and cartilage explants were stimu

72 Monolayer, primary cultures of lapine articular chondrocytes and cartilage slices were studied

73 Cultures of human articular chondrocytes and cartilage tissue slices were

74 Articular chondrocytes and cartilage tissue slices were

75 ctivity was constitutively present in normal articular chondrocytes and cartilage, but decreased in O

76 dy examines the expression of TSG-6 in human articular chondrocytes and cartilage.

77 r IL-1 to stimulate collagenase 1 (MMP-1) in articular chondrocytes and chondrosarcoma cells and foun

78 atory molecules not only in the blood but in articular chondrocytes and fibroblast-like synoviocytes

79 is abundantly expressed by superficial zone articular chondrocytes and has been noted to both be sen

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

81 Primary articular chondrocytes and immortalized chondrocytes (ts

82 We studied cultured human articular chondrocytes and immortalized costal chondrocy

83 d expression of PPi was assessed in cultured articular chondrocytes and immortalized NTPPPH-deficient

84 etalloproteinase expression in primary human articular chondrocytes and in fibroblast-like synovial c

85 signaling in normal and osteoarthritic human articular chondrocytes and investigated the effects of o

86 i-induced catabolic gene expression in human articular chondrocytes and is sufficient to attenuate MM

87 ) to exert degradative effects in both human articular chondrocytes and IVD tissue via upregulation o

88 Articular chondrocytes and meniscal tissue were also inf

89 cell-polymer constructs consisting of bovine articular chondrocytes and polyglycolic acid scaffolds w

90 elevation of TGase activity levels in aging articular chondrocytes and postulated a role for TGase i

91 It stimulates catabolic events in articular chondrocytes and prevents chondrogenic precurs

92 n, reduce levels of phosphorylated VEGFR2 in articular chondrocytes and synovial cells and reduce lev

93 lymerase chain reaction using RNA from human articular chondrocytes and synovial fibroblasts stimulat

94 nction induces matrix-degrading proteases in articular chondrocytes and synoviocytes, stimulating art

95 ulation of superficial zone protein (SZP) in articular chondrocytes and synoviocytes.

96 of SZP accumulation in both superficial zone articular chondrocytes and synoviocytes.

97 erfamily members is regulated differently in articular chondrocytes and synoviocytes.

98 Articular chondrocytes and TC28 cells respired at compar

99 that Rev-ErbAalpha is highly expressed in OA articular chondrocytes and that its expression is modula

100 Isolated human articular chondrocytes and the chondrosarcoma cell line

101 1 gene (Matn1) to investigate the origins of articular chondrocytes and the development of the knee j

102 so required for postnatal differentiation of articular chondrocytes and the timely ossification of bo

103 Cell fractionation studies of primary bovine articular chondrocytes and transfected COS cells suggest

104 We detected TLR2 expression in normal articular chondrocytes and up-regulation of TLR2 in oste

105 ytes was 6.0 +/- 0.6 units/mg protein in old articular chondrocytes and was undetectable in young cho

106 sensitive pool at the cell surface of bovine articular chondrocytes and within a hyaluronidase-insens

107 r findings indicate that TRPV4 is present in articular chondrocytes, and chondrocyte response to hypo

108 n normal knee cartilage samples and cultured articular chondrocytes, and in cartilage specimens from

109 ilages in situ, in untreated cultured normal articular chondrocytes, and in TC28 cells.

110 r levels in human MSC as compared with human articular chondrocytes, and its expression declined duri

111 omechano-TRP channel, is highly expressed in articular chondrocytes, and loss of TRPV4 function is as

112 analyzed human cartilages and cultured human articular chondrocytes, and used recombinant human S100A

113 ains, generated in situ, are internalized by articular chondrocytes, and whether these events are dep

114 of Matn1-Cre/R26R crosses demonstrated that articular chondrocytes are derived from cells that have

115 Articular chondrocytes are distinct in producing lower l

116 tends previous observations that superficial articular chondrocytes are highly specialized cells.

117 Articular chondrocytes are surrounded by an extracellula

118 ns were aggregated with HA and then added to articular chondrocytes, articular chondrocytes transfect

119 enic mice exhibited 50% p38 MAPK activity in articular chondrocytes as compared with WT mice.

120 luronan in cartilage matrix retention, human articular chondrocytes as well as cartilage slices were

121 atrix synthesis and SOX9 expression of human articular chondrocytes at both the gene and protein leve

122 al joint development is the specification of articular chondrocytes at the joint surface.

123 Monolayer cultured primary bovine articular chondrocytes (BACs) were subjected to cyclic t

124 ine-mediated cartilage matrix destruction in articular chondrocytes, believed to be an underlying fac

125 roscale tissue organization regulates bovine articular chondrocyte biosynthesis.

126 gulate metalloproteinase expression in human articular chondrocytes but did mediate prolonged activat

127 constitutively expressed by primary cultured articular chondrocytes, but only CILP-1 expression was d

128 most likely exerts anabolic effects in human articular chondrocytes by activating FGFR3, increasing m

129 ed MT4-MMP with ADAMTS-4 was also induced in articular chondrocytes by HA oligosaccharides.

130 MMP-13 expression was also induced in articular chondrocytes by hyaluronan (HA) hexasaccharide

131 S100A4 expression was detected in human articular chondrocytes by immunoblotting and appeared to

132 We found that lysis of articular chondrocytes by PBMC or polyclonal NK cells wa

133 acilitated glucose transport in normal human articular chondrocytes by proinflammatory cytokines.

134 was applied to monolayer cultures of porcine articular chondrocytes by using a Flexercell strain unit

135 Transfer of growth factor genes to articular chondrocytes can greatly increase matrix synth

136 Inhibition of beta-catenin signaling in articular chondrocytes causes increased cell apoptosis a

137 itative polymerase chain reaction with human articular chondrocytes compared with human mesenchymal s

138 icroscopy with immunofluorescent staining of articular chondrocytes confirmed preferential plasma mem

139 ed gene expression and phenotypic changes in articular chondrocytes culminate in progressive loss of

140 lic events and stimulated anabolic events in articular chondrocytes cultured in an inflammatory envir

141 ated by exposing normal (nonarthritic) human articular chondrocyte cultures to 20% oxygen and 1% oxyg

142 -5 weeks to primary cultures of normal human articular chondrocytes derived from the femoral head car

143 d with rapid changes in PTHrP expression and articular chondrocyte differentiation.

144 a/Smad3 signals are essential for repressing articular chondrocyte differentiation.

145 IOX2, a specific inhibitor of PHD2, promoted articular chondrocyte differentiation.

146 or Sox5/6 in promoting both growth plate and articular chondrocyte differentiation.

147 ESET knock-out did not affect generation of articular chondrocytes during embryonic development.

148 ated inflammatory pathomechanism, in porcine articular chondrocytes exposed to IL-1a, we discovered t

149 Articular chondrocytes express functional RAGE.

150 e confirm that both synovial fibroblasts and articular chondrocytes express MMP-10 following treatmen

151 This study confirms that normal human articular chondrocytes express neutrophil collagenase or

152 Human articular chondrocytes express varying levels of exon 19

153 Normal human knee articular chondrocytes expressed AMPKalpha1, alpha2, bet

154 bserved that normal human and bovine primary articular chondrocytes expressed both IL-8Rs (CXCR1, CXC

155 Adult human articular chondrocytes expressed endogenous PPT mRNA, su

156 ee chondrocytes lacking one of the two known articular chondrocyte-expressed TG isoenzymes (TG2) demo

157 Articular chondrocytes from fetal, adolescent, and adult

158 Articular chondrocytes from IRF-1-/- mice produced simil

159 ature articular cartilage, TGase activity in articular chondrocytes from old and young pigs and in th

160 A study of gene expression in articular chondrocytes from osteoarthritis (OA) patients

161 Creb5 promotes the generation of articular chondrocytes from perichondrial precursors in

162 , inhibits rates of glycolysis, and prevents articular chondrocytes from producing extracellular matr

163 deletion through Cre transfection in primary articular chondrocytes from Rela(fl/fl) mice.

164 tenance of articular cartilage by preventing articular chondrocytes from terminal differentiation and

165 easured with a radiometric assay in cultured articular chondrocytes from the knee joints of old (3-5

166 Using primary cultures of articular chondrocytes from the knee, we defined the fun

167 cartilage explants and immature primary knee articular chondrocytes from TLR-2/TLR-4-double-knockout,

168 Analysis of primary cultures of TMJ articular chondrocytes from wild-type and Ddr2(slie/slie

169 However, the specific role of Runx2 in articular chondrocyte function and in OA development in

170 eletion (Adseverin(-/-)) in mice compromised articular chondrocyte function, by reducing F-actin and

171 ermine the role of beta-catenin signaling in articular chondrocyte function, we generated Col2a1-ICAT

172 anges in growth factor protein production by articular chondrocytes generally corresponded to the cha

173 In addition, human articular chondrocytes (HAC) were treated in vitro with

174 Human articular chondrocytes (HACs) and SW-1353 chondrosarcoma

175 a role in the calcification process of human articular chondrocytes (hACs).

176 attempts at differentiating human ESCs into articular chondrocytes have been unsuccessful.

177 In conclusion, IL-8 and GROalpha induce articular chondrocyte hypertrophy and calcification thro

178 pendent mechanisms promote Cbfa1 expression, articular chondrocyte hypertrophy, and calcification.

179 be rapidly up-regulated in subcultured human articular chondrocytes if grown in alginate, in monolaye

180 tant role of hypertrophic differentiation of articular chondrocytes in calcium crystal deposition.

181 ndrocytes are stable and comparable to adult articular chondrocytes in global gene expression, extrac

182 The number of apoptotic articular chondrocytes in MPS VI rats was similarly redu

183 wth factor-beta1 (TGF-beta1) to adult bovine articular chondrocytes in primary culture and measured t

184 ath and cytotoxicity were evaluated in human articular chondrocytes in response to various NO donor c

185 alyze the effects of SOD2 depletion in human articular chondrocytes in terms of changes to oxidation

186 oles in the (re)generation and maturation of articular chondrocytes in the hyaline cartilage of both

187 tion factor 5 were used to delete PTHrP from articular chondrocytes in the mid-region of mouse articu

188 ular cartilage, these cells take the form of articular chondrocytes in the midzone.

189 Mechanical stimulation of human articular chondrocytes in vitro results in increased lev

190 Nivalenol (NIV) on the metabolism of bovine articular chondrocytes in vitro.

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

192 expression of several genes in normal human articular chondrocytes including inducible nitric oxide

193 Resistin-treated human articular chondrocytes increased the expression of cytok

194 In articular chondrocytes, inhibition of MEK had no effect,

195 Because miR-146a expression in articular chondrocytes is associated with osteoarthritis

196 growing and adult mice, PTHrP expression in articular chondrocytes is load-induced, and unloading is

197 elated to the extracellular matrix in single articular chondrocytes is modified by compressive forces

198 capacity for cartilage repair in human adult articular chondrocytes is severely compromised by minima

199 Human articular chondrocytes isolated from ankle cartilage wer

200 Human articular chondrocytes isolated from cadaveric donors (m

201 Human articular chondrocytes isolated from normal ankle and kn

202 they were phenotypically unique from hyaline articular chondrocytes isolated from the knee joint.

203 TNFalpha or cartilage destruction, in murine articular chondrocytes isolated from wild-type mice and

204 Human articular chondrocytes, isolated from normal ankle carti

205 rkA signaling were examined in human healthy articular chondrocytes maintained under conditions suppo

206 PTHrP may regulate articular chondrocyte maintenance in mice.

207 s that PTHrP might have a regulatory role in articular chondrocyte maintenance.

208 with the development of osteoarthritis (OA), articular chondrocytes may become unresponsive to growth

209 In primary articular chondrocytes, mechanically evoked Ca(2+) trans

210 ndertaken to investigate the role of O(2) in articular chondrocyte metabolism.

211 ion of a natural CD44 decoy-like receptor by articular chondrocytes modulates the function of this ma

212 ontribution of growth plate chondrocytes and articular chondrocytes, not only for long bone growth, b

213 l cells of the developing vasculature and in articular chondrocytes of developing bone.

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

215 ession of the ICAT transgene was detected in articular chondrocytes of the transgenic mice.

216 Bovine articular chondrocytes or bovine cartilage tissue was pr

217 Treatment of human articular chondrocytes or C-28/I2 cells with various cat

218 und to FITC-HA were cointernalized in bovine articular chondrocytes or COS-7 cells transfected with C

219 u with a suspension of cells (primary bovine articular chondrocytes) or cell-free medium and delivere

220 dy was to determine whether TGase from aging articular chondrocytes participates in LTGFbeta activati

221 d-type and knock-out mice indicated that the articular chondrocyte phenotype in ESET-null mutants is

222 e a reproducible model that mimics the adult articular chondrocyte phenotype, particularly in alginat

223 essential for hypoxic induction of the human articular chondrocyte phenotype.

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

225 treatment, indicating the presence of latent articular chondrocyte progenitor cells.

226 Human articular chondrocytes rapidly lose their phenotype in m

227 Healthy articular chondrocytes release ACVs into conditioned med

228 Sox5(fl/fl)6(fl/fl)Gdf5Cre articular chondrocytes remain undifferentiated, as shown

229 The exact molecular mechanisms governing articular chondrocytes remain unknown in skeletal biolog

230 Using RNA sequencing we identified a human articular chondrocyte repertoire of lncRNAs from normal

231 Because articular chondrocytes reside in a hypoxic milieu, anaer

232 Articular chondrocytes respond to mechanical forces by a

233 n the differentiation of organized layers of articular chondrocytes, similar to the organization of m

234 w that adenoviral overexpression of TAK1a in articular chondrocytes stimulated type II collagen prote

235 50 mM) inhibits Hedgehog signaling in bovine articular chondrocytes such that the induction of GLI1 a

236 rtrophic differentiation in growth plate and articular chondrocytes, suggesting a role for TGF-beta i

237 oforms 1 and 8 were highly expressed only in articular chondrocytes, suggesting their splice-specific

238 Monolayer cultures of articular chondrocytes synthesize large amounts of nitri

239 poptosis in all preparations of normal human articular chondrocytes tested.

240 sis of cartilage-specific molecules by human articular chondrocytes than are other factors tested for

241 In its first reported application in human articular chondrocytes, the RNA interference method was

242 pic differences between superficial and deep articular chondrocytes, these studies investigated NO pr

243 In articular chondrocytes, this cell signaling is mediated

244 tor DKK1 induced de-differentiation of human articular chondrocytes through simultaneous activation o

245 of LfcinB-mediated genetic response in human articular chondrocytes, tissue inhibitor of metalloprote

246 tial for innate immunity at the level of the articular chondrocyte to directly contribute to inflamma

247 easured the ability of old and young porcine articular chondrocytes to activate 10 ng/ml of LTGFbeta1

248 when activated, cause the normally quiescent articular chondrocytes to become activated and undergo a

249 The ability of articular chondrocytes to carry out pH homeostasis is co

250 e results show that susceptibility of normal articular chondrocytes to lysis by NK cells is modulated

251 n in human skin and synovial fibroblasts and articular chondrocytes to suppress IL-1-induced expressi

252 is study were to identify miRNA expressed in articular chondrocytes, to determine changes in osteoart

253 RT-PCR demonstrated that human articular chondrocytes transcribe messenger RNA for the

254 ine articular cartilage chondrocytes, bovine articular chondrocytes transfected with a dominant-negat

255 HA and then added to articular chondrocytes, articular chondrocytes transfected with CD44delta67, or

256 Nuclear extracts from bovine articular chondrocytes treated with HA(6) were subjected

257 Furthermore, articular chondrocytes treated with OA derived extracell

258 In osteoarthritis (OA) articular chondrocytes undergo phenotypic changes culmin

259 nockdown of Hif-1alpha expression in primary articular chondrocytes using lentiviral vectors containi

260 domains bound to HA) can be internalized by articular chondrocytes via a mechanism involving HA/CD44

261 SMase down-regulates type II collagen in articular chondrocytes via activation of the ERK signali

262 n of matrix metalloproteinase 13 (MMP-13) by articular chondrocytes via receptor for advanced glycati

263 ther with HMWHA inhibits catabolic events in articular chondrocytes via the inhibition of p38 mitogen

264 glutaminase in adult, but not young, porcine articular chondrocytes was able to activate latent trans

265 of each HAS mRNA expressed in cultured human articular chondrocytes was determined using quantitative

266 A significant increase in cell apoptosis in articular chondrocytes was identified by TUNEL staining

267 medium from IL-1beta and P15-1-treated human articular chondrocytes was less inhibitory for chondroge

268 The rate of oxygen consumption by bovine articular chondrocytes was measured in vitro, either in

269 )/lubricin, a marker of the superficial zone articular chondrocyte, was not detectable under identica

270 To test whether ESET regulates articular chondrocytes, we carried out mesenchyme-specif

271 In the present study, using human articular chondrocytes, we show that intracellular S100A

272 MMP-13 messenger RNA (mRNA) in primary human articular chondrocytes were assessed by real-time polyme

273 levels of phosphorylated STAT1 and STAT3 in articular chondrocytes were corrected.

274 Human articular chondrocytes were cultured in alginate beads o

275 Normal human articular chondrocytes were cultured with or without int

276 Human articular chondrocytes were cultured with resistin.

277 and matrix metalloproteinase 13 (MMP-13) in articular chondrocytes were examined by in situ hybridiz

278 Human OA articular chondrocytes were examined for miR-146b expres

279 Primary rat articular chondrocytes were exposed to biomechanical sig

280 Human articular chondrocytes were found to express all three l

281 Human articular chondrocytes were found to respond to the 120-

282 Primary adult articular chondrocytes were immortalized with a retrovir

283 Monolayer cultures of rabbit articular chondrocytes were infected with recombinant ad

284 Articular chondrocytes were isolated from 3 distinct zon

285 Human articular chondrocytes were isolated from the femoral he

286 Matrix proteins in cultured primary articular chondrocytes were labeled with [(3)H]proline,

287 Isolated bovine articular chondrocytes were maintained in serum-suppleme

288 es obtained from PPT knockout mice and human articular chondrocytes were mechanically stimulated in t

289 hypertrophy, proliferation, and apoptosis of articular chondrocytes were seen in the articular cartil

290 Bovine articular chondrocytes were stimulated with sphingomyeli

291 Primary articular chondrocytes were treated with interleukin-1be

292 In articular chondrocytes, which have a phenotype similar t

293 ly demethylated following treatment of human articular chondrocytes with 10 muM DNA-methyltransferase

294 Treatment of freshly isolated normal human articular chondrocytes with an agonistic Fas antibody in

295 Transfection of bovine articular chondrocytes with CD44Delta67 also inhibited p

296 Stimulation of normal human articular chondrocytes with IL-17 induced nitric oxide (

297 Treatment of articular chondrocytes with known catabolic agents resul

298 t through inhibition of DNA binding in human articular chondrocytes, with decreased expression of sev

299 Articular chondrocytes within cartilage explants and enz

300 Upon ectopic expression in primary human articular chondrocytes, Wnt7a inhibited IL-1beta-induced