ライフサイエンスコーパス: articular chondrocyte

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

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

3 ttermates and in primary chicken and porcine articular chondrocytes.

4 mbers and activins than are superficial zone articular chondrocytes.

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

6 ynovial lining, subsynovial vasculature, and articular chondrocytes.

7 ory cytokines or by fibronectin fragments in articular chondrocytes.

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

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

10 enhances cartilage matrix synthesis by human articular chondrocytes.

11 d transfection of primary and passaged human articular chondrocytes.

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

13 A from SW1353 chondrocytes and primary human articular chondrocytes.

14 ial cells divide more slowly than underlying articular chondrocytes.

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

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

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

18 development of methods to direct vectors to articular chondrocytes.

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

20 inflammation and altered differentiation of articular chondrocytes.

21 However, RANKL does not activate human articular chondrocytes.

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

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

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

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

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

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

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

29 marily responsible for HA synthesis in human articular chondrocytes.

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

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

32 1 and 2 stimulate the metabolic activity of articular chondrocytes.

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

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

35 ecently been demonstrated to be expressed in articular chondrocytes.

36 tibody to PTHrP increased PPi elaboration by articular chondrocytes.

37 i accumulation versus proliferation in human articular chondrocytes.

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

39 the spherical configuration of primary human articular chondrocytes.

40 V4 transduces dynamic compressive loading in articular chondrocytes.

41 the cartilage, and enhanced proliferation of articular chondrocytes.

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

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

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

45 flammatory and chondroprotective cytokine in articular chondrocytes.

46 DOT1L is also expressed in OA articular chondrocytes.

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

48 ation in surface zone cartilage and isolated articular chondrocytes.

49 expression was detected in rodent and human articular chondrocytes.

50 matrix-degrading enzyme production in human articular chondrocytes.

51 growth chondrocytes and is also expressed in articular chondrocytes.

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

53 l-mediated cytotoxicity against normal human articular chondrocytes.

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

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

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

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

58 Human articular chondrocytes actively produce reactive oxygen

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

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

61 Articular chondrocyte and cartilage cultures were stimul

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

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

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

65 Human articular chondrocytes and cartilage explants (obtained

66 Human articular chondrocytes and cartilage explants were stimu

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

68 Cultures of human articular chondrocytes and cartilage tissue slices were

69 Articular chondrocytes and cartilage tissue slices were

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

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

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

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

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

75 Primary articular chondrocytes and immortalized chondrocytes (ts

76 We studied cultured human articular chondrocytes and immortalized costal chondrocy

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

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

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

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

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

82 Articular chondrocytes and meniscal tissue were also inf

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

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

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

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

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

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

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

90 Articular chondrocytes and TC28 cells respired at compar

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

92 Isolated human articular chondrocytes and the chondrosarcoma cell line

93 1 gene (Matn1) to investigate the origins of articular chondrocytes and the development of the knee j

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

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

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

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

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

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

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

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

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

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

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

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

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

107 Articular chondrocytes are distinct in producing lower l

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

109 Articular chondrocytes are surrounded by an extracellula

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

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

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

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

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

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

116 roscale tissue organization regulates bovine articular chondrocyte biosynthesis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 -5 weeks to primary cultures of normal human articular chondrocytes derived from the femoral head car

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

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

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

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

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

138 Articular chondrocytes express functional RAGE.

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

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

141 Human articular chondrocytes express varying levels of exon 19

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

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

144 Adult human articular chondrocytes expressed endogenous PPT mRNA, su

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

146 Articular chondrocytes from fetal, adolescent, and adult

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

185 Human articular chondrocytes isolated from ankle cartilage wer

186 Human articular chondrocytes isolated from cadaveric donors (m

187 Human articular chondrocytes isolated from normal ankle and kn

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

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

190 Human articular chondrocytes, isolated from normal ankle carti

191 PTHrP may regulate articular chondrocyte maintenance in mice.

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

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

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

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

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

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

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

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

200 Bovine articular chondrocytes or bovine cartilage tissue was pr

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

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

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

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

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

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

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

208 Human articular chondrocytes rapidly lose their phenotype in m

209 Healthy articular chondrocytes release ACVs into conditioned med

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

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

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

213 Because articular chondrocytes reside in a hypoxic milieu, anaer

214 Articular chondrocytes respond to mechanical forces by a

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

216 50 mM) inhibits Hedgehog signaling in bovine articular chondrocytes such that the induction of GLI1 a

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

218 Monolayer cultures of articular chondrocytes synthesize large amounts of nitri

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

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

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

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

223 In articular chondrocytes, this cell signaling is mediated

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

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

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

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

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

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

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

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

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

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

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

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

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

237 Furthermore, articular chondrocytes treated with OA derived extracell

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

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

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

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

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

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

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

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

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

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

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

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

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

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

252 Human articular chondrocytes were cultured in alginate beads o

253 Normal human articular chondrocytes were cultured with or without int

254 Human articular chondrocytes were cultured with resistin.

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

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

257 Primary rat articular chondrocytes were exposed to biomechanical sig

258 Human articular chondrocytes were found to express all three l

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

260 Primary adult articular chondrocytes were immortalized with a retrovir

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

262 Articular chondrocytes were isolated from 3 distinct zon

263 Human articular chondrocytes were isolated from the femoral he

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

265 Isolated bovine articular chondrocytes were maintained in serum-suppleme

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

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

268 Bovine articular chondrocytes were stimulated with sphingomyeli

269 Primary articular chondrocytes were treated with interleukin-1be

270 In articular chondrocytes, which have a phenotype similar t

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

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

273 Transfection of bovine articular chondrocytes with CD44Delta67 also inhibited p

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

275 Treatment of articular chondrocytes with known catabolic agents resul

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

277 Articular chondrocytes within cartilage explants and enz

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