ライフサイエンスコーパス: synovial fibroblast

1 these cells shared features of inflammatory synovial fibroblasts.

2 al properties of key cells in RA, especially synovial fibroblasts.

3 tern of cytokine and chemokine production in synovial fibroblasts.

4 potent inhibitors of IL-34 expression in RA synovial fibroblasts.

5 on of RANKL and OPG in both human and murine synovial fibroblasts.

6 lso inhibited in IL-1alpha-stimulated rabbit synovial fibroblasts.

7 d IL-1alpha-induced p-ERK levels in human RA synovial fibroblasts.

8 etalloproteinases, and hyperproliferation of synovial fibroblasts.

9 es and osteoblast-like cells, in addition to synovial fibroblasts.

10 EGCG was nontoxic to RA synovial fibroblasts.

11 location of NF-kappaB in IL-1beta-treated RA synovial fibroblasts.

12 on, in close proximity to hyperproliferating synovial fibroblasts.

13 the inactive Rb isoform compared with non-RA synovial fibroblasts.

14 nduced production of IL-6 or MMP-1 in non-RA synovial fibroblasts.

15 V transcripts are expressed and inducible in synovial fibroblasts.

16 sion of FLIP is regulated by NF-kappaB in RA synovial fibroblasts.

17 , leading to decreased MMP-1 secretion in RA synovial fibroblasts.

18 ented 27% of the total message population in synovial fibroblasts.

19 ctivity, inhibits IL-6, MMP-1, and p38 in RA synovial fibroblasts.

20 tected on RA SF lymphocytes, macrophages, or synovial fibroblasts.

21 arrest, decreases IL-6 synthesis in p21-null synovial fibroblasts.

22 xpression of proinflammatory molecules in RA synovial fibroblasts.

23 d activation of AP-1 compared with wild-type synovial fibroblasts.

24 rs was detectable on RA SF lymphocytes or RA synovial fibroblasts.

25 ted RA synovial fibroblasts compared with OA synovial fibroblasts.

26 ces in expression between RA- and OA-derived synovial fibroblasts.

27 CR4 was expressed by chondrocytes but not by synovial fibroblasts.

28 ions leading to the invasive phenotype of RA-synovial fibroblasts.

29 ntially modify activation of ERKs or JNKs in synovial fibroblasts.

30 lso activated MMP-1 transcription in primary synovial fibroblasts.

31 nduced an invasive phenotype in normal human synovial fibroblasts.

32 unction, was readily adaptable for assays of synovial fibroblasts.

33 th pro- and anti-inflammatory actions, in RA synovial fibroblasts.

34 CAM-1 expression on endothelial cells and RA synovial fibroblasts.

35 o induce invasive properties in normal human synovial fibroblasts.

36 o B19 and phenotypic changes in normal human synovial fibroblasts.

37 fabricated by using 1.0% alginate and rabbit synovial fibroblasts.

38 mphocytes and APCs as well as hyperplasia of synovial fibroblasts.

39 d MMP-1 production in human chondrocytes and synovial fibroblasts.

40 elysin, as well as PGE2 production, in human synovial fibroblasts.

41 pression of the collagenase-1 gene in rabbit synovial fibroblasts.

42 paracrine pathways involving macrophages and synovial fibroblasts.

43 aling receptor is up-regulated on rheumatoid synovial fibroblasts.

44 tch target genes are markedly upregulated in synovial fibroblasts.

45 ys using a coculture system of HMVECs and RA synovial fibroblasts.

46 to-cell adhesion molecule expressed on joint synovial fibroblasts.

47 highest expression found in macrophages and synovial fibroblasts.

48 fibroblasts, we examined BRAF in rheumatoid synovial fibroblasts.

49 f sumoylation for resistance to apoptosis in synovial fibroblasts.

50 pha, by regulating the ERK-1/2 pathway in RA synovial fibroblasts.

51 of the melanocortin type 1 receptor (MC(1)), synovial fibroblasts acquire a senescence phenotype char

52 y indicate that visfatin/PBEF is involved in synovial fibroblast activation by triggering fibroblast

53 45RA(+) all had comparable ability to induce synovial fibroblast activation.

54 Synovial fibroblasts also invaded into cartilage in an M

55 The synovial fibroblasts also promote inflammation in the sy

56 nd suppressed IL-6 and MMP-1 secretion in RA synovial fibroblasts, although the steady-state levels o

57 pecifically abrogated Mcl-1 expression in RA synovial fibroblasts and affected Mcl-1 expression to a

58 We confirm that both synovial fibroblasts and articular chondrocytes express

59 ukin (IL)-4 has been shown in human skin and synovial fibroblasts and articular chondrocytes to suppr

60 ODF is expressed by both synovial fibroblasts and by activated T lymphocytes deri

61 PS rats, cats, and/or dogs revealed that MPS synovial fibroblasts and fluid displayed elevated expres

62 MEFV product, was determined in transfected synovial fibroblasts and HeLa cells with plasmids encodi

63 FKN was expressed on cultured synovial fibroblasts and hyperplastic synoviocytes in th

64 , ODF mRNA was detected in cultured adherent synovial fibroblasts and in activated T lymphocytes deri

65 ects of the inhibitor in cytokine-stimulated synovial fibroblasts and in cytokine-induced arthritis i

66 ed matrix metalloproteinase-2 activity in RA synovial fibroblasts and in joint homogenates, possibly

67 The presence of cathepsin K polypeptide in synovial fibroblasts and macrophage-like cells in normal

68 n to explore the roles of hyperproliferating synovial fibroblasts and macrophages in abnormal osteocl

69 tial role of IL-17 in monocyte migration, RA synovial fibroblasts and macrophages were activated with

70 CP-1, which were significantly induced in RA synovial fibroblasts and macrophages.

71 Of note is the expression of cathepsin K in synovial fibroblasts and mononuclear macrophage-like cel

72 ified by real-time quantitative PCR in human synovial fibroblasts and murine mesenchymal stem cells.

73 athway resulted in impaired proliferation of synovial fibroblasts and partial attenuation of the prot

74 cripts were induced by lipopolysaccharide in synovial fibroblasts and PBLs.

75 , as well as decreased lubricin synthesis by synovial fibroblasts and superficial zone chondrocytes.

76 ere used to assess p-ERK in human and rabbit synovial fibroblasts and synovial tissue from rheumatoid

77 he joint-specific origins of mouse and human synovial fibroblasts and synovial tissues.

78 se involve the stimulation of mitogenesis in synovial fibroblasts and the secretion of metalloprotein

79 herefore studied the production of ADAMTS by synovial fibroblasts and their contribution to cartilage

80 ong (FLIP(L)) and FLIP short (FLIP(S)) in RA synovial fibroblasts and to determine the role of FLIP i

81 ovial membrane as well as a proliferation of synovial fibroblasts and vascular cells.

82 y mRNA for ODF in synovial tissues, adherent synovial fibroblasts, and activated T lymphocytes derive

83 rs were used to infect RA ST explants and RA synovial fibroblasts, and conditioned medium (CM) was co

84 CD56(dim) both in vitro, in the presence of synovial fibroblasts, and in vivo, upon transfer into NO

85 types (human Saos2 osteosarcoma cells, human synovial fibroblasts, and rat mesenchymal stem cells) wi

86 ocytes/macrophages, B and T lymphocytes, and synovial fibroblasts, and TLR-induced MIF transcription

87 cytokine production, an ability to activate synovial fibroblasts, and to survive and persist in the

88 y co-culture of WT but not ST2(-/-) MCs with synovial fibroblasts, and was blocked by antibodies agai

89 delivery of TRAIL to induce macrophage or RA synovial fibroblast apoptosis was examined by flow cytom

90 gen citrullination decreased the adhesion of synovial fibroblasts approximately 50% (P<0.05) and mese

91 treatment for rheumatoid arthritis (RA), and synovial fibroblasts are a major IL-6 producer in the in

92 system, and the availability of adult human synovial fibroblasts are likely to provide new pathophys

93 ed in the joints of patients with RA, yet RA synovial fibroblasts are relatively resistant to apoptos

94 from the cytosol to the nucleus of human RA synovial fibroblasts, as well as NF-kappaB activation me

95 The inhibitory activity in the synovial fibroblast assay correlated with the rate of in

96 Mcl-1 was critical for the survival of RA synovial fibroblasts, because the forced reduction of Mc

97 appears to profoundly affect chondrocyte and synovial fibroblast biology, including cell survival, in

98 ted MMP-1 and MMP-3 protein production by RA synovial fibroblasts, both alone and in synergy with tum

99 ynovium, since SDF-1 mRNA was synthesized by synovial fibroblasts but not by chondrocytes.

100 on the survival of normal macrophages or RA synovial fibroblasts but readily induced apoptosis in th

101 MEFV was expressed in synovial fibroblasts, but not in chondrocytes.

102 ear cell-recruiting chemokines uniquely from synovial fibroblasts, but not matched skin fibroblasts,

103 ced IL-6 production and transsignaling in RA synovial fibroblasts by inducing alternative splicing of

104 Recently it has been found that synovial fibroblasts can also function as accessory cell

105 a2M-methylamine to rheumatoid but not normal synovial fibroblasts caused a rapid rise in inositol 1,4

106 ron on the proliferation of a primary, human synovial fibroblast cell (HSFC) line and the involvement

107 ugh increased proliferation and/or decreased synovial fibroblast cell death.

108 ion in both primary RA SF and the rheumatoid synovial fibroblast cell line, MH7A.

109 EGCG effects on cultured RA synovial fibroblast cell morphology, proliferation, and

110 e for cytokine-mediated activation of Sp1 in synovial fibroblast cells and its participation in regul

111 through induction of collagenase activity in synovial fibroblast cells that line the joint tissues.

112 MEFV messenger RNA in synovial fibroblasts, chondrocytes, and peripheral blood

113 ed by IL-1beta and TNFalpha in cells such as synovial fibroblasts, chondrocytes, osteoblasts, and mon

114 xtent, in OA, and is specifically induced in synovial fibroblasts, chondrocytes, osteoblasts, and mon

115 on, ADAM-10 siRNA-treated HMVECs from the RA synovial fibroblast coculture system had decreased endot

116 ession of p21 is also reduced in isolated RA synovial fibroblasts compared with OA synovial fibroblas

117 We reported that synovial fibroblasts constitutively express and release

118 flammatory response, mediated by chondrocyte-synovial fibroblast cross-talk, was enhanced by the obes

119 Compared with normal synovial fibroblasts, cultured RA fibroblast-like synovi

120 ition of rHuIL-15 at 10-100 ng/ml to primary synovial fibroblast cultures failed to up-regulate expre

121 2-fold) of cathepsin K (P < 0.05) in primary synovial fibroblast cultures, without differences in exp

122 dentify active cathepsin K enzyme in primary synovial fibroblast cultures.

123 found that human RA and osteoarthritis (OA) synovial fibroblasts derived from independent donors rep

124 he induction of proinflammatory cytokines by synovial fibroblasts derived from rheumatoid arthritis (

125 CD4(+) T cells to TH17 cells was mediated by synovial fibroblast-derived IL-6.

126 In synovial fibroblasts, dermal fibroblasts, and HUVECs, IK

127 Synovial fibroblasts destroy articular cartilage and bon

128 Additionally, p21-null synovial fibroblasts display enhanced activation of AP-1

129 Quiescent RA, compared with non-RA synovial fibroblasts, displayed a 200% (P < 0.02) increa

130 In RA synovial fibroblasts, EGCG (5-50 microM) inhibited const

131 tein coupled receptor promotes senescence in synovial fibroblasts, enabling amelioration of joint inf

132 Tissue TSP2, produced by synovial fibroblasts, endothelial cells, and macrophages

133 odel of RA, and that it does so by targeting synovial fibroblasts, endothelial cells, and osteoclasts

134 Our results indicate that synovial fibroblasts exhibit a positional identity that

135 Proliferating RA synovial fibroblasts exhibited a 60% (P < 0.12) increase

136 B19 serum-treated synovial fibroblasts exhibited an increase in invasion o

137 During osteoarthritis, synovial fibroblasts exposed to anomalous mechanical for

138 RA synovial fibroblasts express high levels of the MAP kina

139 Primary cell cultures of RA- and OA-derived synovial fibroblasts expressed comparable amounts of cat

140 TNF induced the production of soluble synovial fibroblast factors that suppressed the macropha

141 Thus, through its activation of synovial fibroblasts, fibrin(ogen) deposition may promot

142 To study the regulation of VCAM-1 in synovial fibroblasts, fibroblast-like synoviocytes (FLS)

143 ssion was confirmed in both chondrocytes and synovial fibroblasts following stimulation with either I

144 Proliferation of synovial fibroblasts, for example, underlies the formati

145 Here we show transcriptomic differences in synovial fibroblasts from different joint locations and

146 ails to induce IL-16 or RANTES expression in synovial fibroblasts from donors with osteoarthritis.

147 However, synovial fibroblasts from obese OA patients were found t

148 IL-33 was expressed in synovial fibroblasts from patients with rheumatoid arthr

149 1 and bone morphogenetic protein (BMP)-2, in synovial fibroblasts from RA patients.

150 Synovial fibroblasts from the rheumatoid joint play an i

151 ther cancers was identified in first passage synovial fibroblasts from two of nine rheumatoid arthrit

152 pase 3 activation by EGCG also suppressed RA synovial fibroblast growth, and this effect was mimicked

153 dividual NF-kappaB subunits, p65 and p50, in synovial fibroblasts harvested from patients with rheuma

154 ogens, and the expression of certain TLRs by synovial fibroblasts has revealed the potential for inna

155 (hyaluronan and lubricin) and cytokines from synovial fibroblasts have been identified.

156 isoforms of FLIP messenger RNA (mRNA) in RA synovial fibroblasts; however, FLIP(L) was the dominant

157 activates the sphingomyelin pathway in human synovial fibroblasts (HSF) and the potential role of cer

158 TNFalpha induced RA synovial fibroblast IL-18BPa and IL-18 in a time-depende

159 oproteinases (MMPs) are enzymes expressed by synovial fibroblasts important for cartilage erosion.

160 -1 beta-induced rheumatoid arthritis-derived synovial fibroblasts in a dose-dependent manner.

161 es increased synthesis of several MMPs by RA synovial fibroblasts in a MAPK- and NF-kappaB-dependent

162 circulating microparticles, which activated synovial fibroblasts in an IL-1-dependent manner.

163 d that gene expression programs regulated by synovial fibroblasts in our coculture system were also r

164 c value in regulating the invasive growth of synovial fibroblasts in RA.

165 data provide further evidence of the role of synovial fibroblasts in regulating the pattern and persi

166 ESE-1 and Ang-1 are induced in synovial fibroblasts in response to inflammatory cytokin

167 ivery of p21 (Ad-p21) arrests both RA and OA synovial fibroblasts in the G(0)/G(1) phase of the cell

168 mediators and induced the repair response of synovial fibroblasts in vitro.

169 oliferation and cytokine production of human synovial fibroblasts in vitro.

170 thogenesis of rheumatoid arthritis (RA), the synovial fibroblasts increase in number and produce proi

171 Ad-CA-MKK3 infection in RA synovial fibroblasts increased p38 phosphorylation, and

172 ecule expression on endothelial cells and RA synovial fibroblasts indicates that IL-18 may contribute

173 is suppressed only in the Ad-p21-infected RA synovial fibroblasts, indicating a novel role for p21 in

174 d rheumatoid synovial tissue and isolated RA synovial fibroblasts invaded into a 3-D collagen matrix

175 Moreover, p21 positivity in the synovial fibroblasts inversely correlates with medium sy

176 Expression of VCAM-1 on synovial fibroblasts is a clinical hallmark of rheumatoi

177 kemia 1 (Mcl-1) in rheumatoid arthritis (RA) synovial fibroblasts is a major cause of their resistanc

178 More importantly, activated synovial fibroblasts isolated from patients with rheumat

179 duced Bcl-2 expression and cell viability in synovial fibroblasts isolated from RA and osteoarthritis

180 Using synovial fibroblasts isolated from RA joints, we found t

181 Besides stimulating synovial fibroblast-like cells to proliferate, BCP cryst

182 sduction was negatively regulated by heme in synovial fibroblast-like synoviocytes from rheumatoid ar

183 Our results suggest that synovial fibroblasts may significantly contribute to bon

184 oth transient and longer duration changes in synovial fibroblast membrane potential.

185 nd NF-kappaB inhibitors partially blocked RA synovial fibroblast MMP expression.

186 Cad-11-Fc stimulation increased RA synovial fibroblast MMP messenger RNA levels.

187 objective of this study was to determine if synovial fibroblast MMP production is regulated by cadhe

188 ranscriptome analysis showed that cocultured synovial fibroblasts modulate the expression of approxim

189 tify the defective cells in BXD2 mice, mouse synovial fibroblasts (MSFs) were cultured with bone marr

190 t, native pyrin was predominantly nuclear in synovial fibroblasts, neutrophils, and dendritic cells,

191 ylated genes between RASF and osteoarthritis synovial fibroblasts (OASF) were identified by methylate

192 t were higher in RASF than in osteoarthritis synovial fibroblasts (OASF), as demonstrated by immunohi

193 as compared between RASFs and osteoarthritic synovial fibroblast (OASFs) using quantitative polymeras

194 thritis (RASF), but not exosomes produced by synovial fibroblasts obtained from individuals with oste

195 study, we show that the exosomes produced by synovial fibroblasts obtained from individuals with rheu

196 ct ex vivo RA synovial membrane cultures and synovial fibroblasts obtained from patients with RA unde

197 The reasons the activation of synovial fibroblasts often persists despite antiinflamma

198 In normal synovial fibroblasts only one site for 125I-alpha2M-meth

199 a lesser extent in osteoarthritis and normal synovial fibroblasts or endothelial cells.

200 and BMP-2 decreased IL-34 expression in the synovial fibroblasts or in murine mesenchymal stem cells

201 The induction of apoptosis of macrophages, synovial fibroblasts or lymphocytes, either through supp

202 The synovial fibroblast, or fibroblast-like synoviocyte (FLS

203 or Northern blotting in human chondrocytes, synovial fibroblasts, osteoblasts, and macrophages, befo

204 nal diversity translates into joint-specific synovial fibroblast phenotypes with distinct adhesive, p

205 tion of exogenous IL-18BPa-Fc reduced the RA synovial fibroblast phosphorylation of ERK-1/2 induced b

206 ssion of p21, a cell cycle inhibitor, in the synovial fibroblast population from RA compared with ost

207 of ion channels that are expressed in human synovial fibroblast preparations have begun to provide i

208 In common with many other cell types, synovial fibroblasts produce exosomes.

209 In rheumatoid arthritis (RA), synovial fibroblasts proliferate excessively, eventually

210 nd activation of endothelial cells, and more synovial fibroblast proliferation.

211 Therefore, synovial fibroblasts provide the biochemical tools to th

212 e, and that it is predominately expressed by synovial fibroblast (RASF) and macrophages in the lining

213 Primary RA synovial fibroblast (RASF) cell lines were transfected i

214 itro, exRNA (150-5000 nt) was released by RA synovial fibroblasts (RASF) under hypoxic conditions but

215 roinflammatory loop upon interaction with RA synovial fibroblasts (RASF), including increased autocri

216 s of human promoters in rheumatoid arthritis synovial fibroblasts (RASF).

217 Rheumatoid arthritis synovial fibroblasts (RASFs) contribute to arthritic car

218 To model RA synovium, RA synovial fibroblasts (RASFs) were cocultured with endoth

219 of histone deacetylase (HDAC) enzymes in RA synovial fibroblasts (RASFs), a key cellular mediator of

220 MP) secretion from rheumatoid arthritis (RA) synovial fibroblasts (RASFs), and whether MMP-1 secretio

221 tterns of RA synovial tissue, focusing on RA synovial fibroblasts (RASFs), key players in RA synovium

222 p90 was characterized in Jurkat cells and RA synovial fibroblasts (RASFs).

223 yptase, a major product of mast cells, on RA synovial fibroblasts (RASFs).

224 n was analyzed in human rheumatoid arthritis synovial fibroblasts (RASFs).

225 During the pathogenesis of RA, synovial fibroblasts reenter the cell cycle and multiply

226 tivation of the MMP-1 gene by IL-1 in rabbit synovial fibroblasts required a dorsal-like element, whi

227 NF-alpha, and IL-1beta treatment of cultured synovial fibroblasts resulted in the increased expressio

228 Analyses of p21-deficient mouse synovial fibroblasts reveal a 100-fold increase in IL-6

229 ing Mcl-1 expression and its mechanism of RA synovial fibroblast sensitization to TNFalpha-induced ap

230 itis (RA) is linked to functional changes in synovial fibroblasts (SF) and local infiltration of T ly

231 levels in relation to RANKL expression in RA synovial fibroblasts (SF) and the development of bone er

232 P-1 secretion from rheumatoid arthritis (RA) synovial fibroblasts (SF) stimulated with TNF-alpha.

233 up-regulation by IL-1 beta, in normal human synovial fibroblasts (SF).

234 howed opposite effects (e.g., osteoarthritis synovial fibroblasts [SF]; GF(-) versus GF(+): 10.7- ver

235 Rheumatoid arthritis (RA) synovial fibroblasts (SFs) are relatively resistant to a

236 Synovial fibroblasts (SFs) play a critical role in the p

237 the influence of the proinflammatory milieu, synovial fibroblasts (SFs), the main effector cells in d

238 the TNF-alpha signaling pathway in human RA synovial fibroblasts (SFs).

239 Synovial fibroblasts share a number of phenotype markers

240 ovium, and skin) to test the hypothesis that synovial fibroblasts share similarities with bone marrow

241 s upstream of PI3-kinase in IL-18-induced RA synovial fibroblast signaling.

242 Binding of alpha2M-methylamine to rheumatoid synovial fibroblasts significantly increased the synthes

243 However, in synovial fibroblasts, STAT3 did not suppress IL-6 produc

244 ng RNA from human articular chondrocytes and synovial fibroblasts stimulated with IL-1 plus OSM or tu

245 in and messenger RNA levels in HMVECs and RA synovial fibroblasts stimulated with proinflammatory med

246 ivation of three distinct pathways during RA synovial fibroblast stimulation: two Src-dependent pathw

247 Cathepsin K protein was localized in synovial fibroblasts, stromal multinucleated giant cells

248 We found that synovial fibroblasts strongly suppressed TNF-mediated in

249 predominantly found in endothelial cells and synovial fibroblasts, suggesting heterotypic signaling b

250 s well as PI 3-kinase to induce VCAM-1 on RA synovial fibroblasts, suggesting that there may be two d

251 he potential to interact with resident joint synovial fibroblasts (synoviocytes) and induce the expre

252 CCL3, and CCL5 was significantly greater in synovial fibroblasts than in skin fibroblasts.

253 IL-18 and IL-18BPa synthesis in RA synovial fibroblasts that had been treated with proinfla

254 f macrophage phenotype as a new function for synovial fibroblasts that may prove to be a contributing

255 Furthermore, in RA synovial fibroblasts the ectopic expression of p21 reduc

256 matoid arthritis (RA-IgG) stimulate in their synovial fibroblasts the expression of these same cytoki

257 ophage response to TNF is regulated by human synovial fibroblasts, the representative stromal cell ty

258 Because IL-33 is derived predominantly from synovial fibroblasts, this finding provides a novel mech

259 matrix metalloproteinase (MMP) expression in synovial fibroblasts through the generation of fibronect

260 Thus, we suggest that cad-11 modulates synovial fibroblasts to evoke inflammatory factors that

261 In support of the latter data, exposure of synovial fibroblasts to hTryptase-beta/heparin or mMCP-6

262 Resting T cells also induced synovial fibroblasts to produce PGE(2), indicating activ

263 Here, we show that cad-11 engagement induces synovial fibroblasts to secret proinflammatory cytokines

264 induces apoptosis and further sensitizes RA synovial fibroblasts to TNFalpha-induced apoptosis by sp

265 The resistance of RA synovial fibroblasts to TNFalpha-induced apoptosis is me

266 gly, Mcl-1 degradation by EGCG sensitized RA synovial fibroblasts to TNFalpha-induced PARP cleavage a

267 ed the synthesis of DNA compared with normal synovial fibroblasts treated similarly.

268 lementary DNA from rheumatoid arthritis (RA) synovial fibroblasts treated with IL-6 and soluble IL-6

269 ecule-1 (ICAM-1) on endothelial cells and RA synovial fibroblasts using flow cytometry.

270 eine) or PI 3-kinase (LY294002) inhibited RA synovial fibroblast VCAM-1 expression by 50 to 60%.

271 lammatory, eliciting cytokine responses from synovial fibroblasts via interleukin-1.

272 nces the cross-talk between chondrocytes and synovial fibroblasts via raised levels of the pro-inflam

273 ytokine-induced inflammatory responses in RA synovial fibroblasts via regulation of the localization

274 T-PHPMA-I to inhibit cathepsin K activity in synovial fibroblasts was also evaluated.

275 -stimulated stromelysin production in rabbit synovial fibroblasts was assessed by enzyme-linked immun

276 AR-2, expression in RA synovium and cultured synovial fibroblasts was characterized.

277 cyte/macrophages, normal macrophages, and RA synovial fibroblasts was examined by flow cytometry with

278 on of costimulatory ligands CD80 and CD86 on synovial fibroblasts was identified as one mechanism of

279 hanism demonstrated that IL-6 secretion from synovial fibroblasts was induced by chondrocyte-derived

280 Primary human synovial fibroblasts were also examined using flow cytom

281 tro experiments with human keratinocytes and synovial fibroblasts were conducted.

282 senger RNA (mRNA) levels in chondrocytes and synovial fibroblasts were determined by reverse transcri

283 Cultures of autologous synovial fibroblasts were established and divided into t

284 RA and non-RA synovial fibroblasts were examined by enzyme-linked immu

285 RA synovial fibroblasts were isolated from RA synovial tiss

286 To mimic cadherin 11 engagement, human RA synovial fibroblasts were stimulated with a chimeric con

287 Cultured human synovial fibroblasts were stimulated with exogenous TNF-

288 SW-1353 cells and rabbit synovial fibroblasts were transfected with a 4.3-kb huma

289 Primary rabbit synovial fibroblasts were transiently transfected with M

290 n vitro system in which normal primary human synovial fibroblasts were treated with or without parvov

291 nce of T cell mitogens, induce activation of synovial fibroblasts when cocultured for 6-24 h.

292 pathogenesis of RA includes the concept that synovial fibroblasts, which are essential to cartilage a

293 ne, in contrast to B19-negative sera-treated synovial fibroblasts, which exhibited no significant cha

294 1 by EGCG triggered caspase 3 activity in RA synovial fibroblasts, which was mediated via down-regula

295 activity of p38 was enhanced by infecting RA synovial fibroblasts with a replication-defective adenov

296 We now demonstrate that coculture of human synovial fibroblasts with fibrin(ogen) results in the up

297 Treatment of normal synovial fibroblasts with GAGs also led to production of

298 blot analysis revealed that coincubation of synovial fibroblasts with IL-1 and IL-4 resulted in a si

299 sion after stimulation of RA- and OA-derived synovial fibroblasts with IL-1 beta and TNF alpha furthe

300 AF-specific siRNA inhibited proliferation of synovial fibroblasts with V600R mutations.