ライフサイエンスコーパス: synovial fibroblast

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

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

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

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

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

6 etalloproteinases, and hyperproliferation of synovial fibroblasts.

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

8 EGCG was nontoxic to RA synovial fibroblasts.

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

10 on, in close proximity to hyperproliferating synovial fibroblasts.

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

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

13 V transcripts are expressed and inducible in synovial fibroblasts.

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

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

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

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

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

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

20 xpression of proinflammatory molecules in RA synovial fibroblasts.

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

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

23 ted RA synovial fibroblasts compared with OA synovial fibroblasts.

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

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

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

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

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

29 nduced an invasive phenotype in normal human synovial fibroblasts.

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

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

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

33 o induce invasive properties in normal human synovial fibroblasts.

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

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

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

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

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

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

40 paracrine pathways involving macrophages and synovial fibroblasts.

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

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

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

44 fibroblasts, we examined BRAF in rheumatoid synovial fibroblasts.

45 f sumoylation for resistance to apoptosis in synovial fibroblasts.

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

47 tern of cytokine and chemokine production in synovial fibroblasts.

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

49 45RA(+) all had comparable ability to induce synovial fibroblast activation.

50 Synovial fibroblasts also invaded into cartilage in an M

51 The synovial fibroblasts also promote inflammation in the sy

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

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

54 We confirm that both synovial fibroblasts and articular chondrocytes express

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

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

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

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

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

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

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

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

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

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

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

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

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

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

69 examined the interaction between isolated RA synovial fibroblasts and normal human cartilage engrafte

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 Human synovial fibroblasts, another prominent cell type in the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

115 We reported that synovial fibroblasts constitutively express and release

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

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

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

119 2-fold) of cathepsin K (P < 0.05) in primary synovial fibroblast cultures, without differences in exp

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

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

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

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

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

125 Synovial fibroblasts destroy articular cartilage and bon

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

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

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

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

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

131 Expression of v-src in synovial fibroblasts enhanced basal and IL-1-inducible t

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

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

134 During osteoarthritis, synovial fibroblasts exposed to anomalous mechanical for

135 RA synovial fibroblasts express high levels of the MAP kina

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

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

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

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

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

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

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

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

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

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

146 1 and bone morphogenetic protein (BMP)-2, in synovial fibroblasts from RA patients.

147 Synovial fibroblasts from the rheumatoid joint play an i

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

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

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

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

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

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

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

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

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

157 -1 beta-induced rheumatoid arthritis-derived synovial fibroblasts in a dose-dependent manner.

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

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

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

161 ils and macrophages), endothelial cells, and synovial fibroblasts in RA synovium.

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

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

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

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

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

167 novial cells, and attachment and invasion of synovial fibroblasts (in)to adjacent cartilage and bone,

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

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

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

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

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

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

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

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

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

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

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

179 We conclude that RA synovial fibroblasts maintain their invasive and destruc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 Therefore, synovial fibroblasts provide the biochemical tools to th

209 ammatory cytokine, which is released from RA synovial fibroblasts (RA-SF).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

227 eta (IL-1beta) up-regulates human rheumatoid synovial fibroblast (RSF) 85-kDa phospholipase A2 (PLA2)

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

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

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

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

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

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

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

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

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

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

238 Synovial fibroblasts share a number of phenotype markers

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

259 role of adhesion molecules in attachment of synovial fibroblasts to cartilage, and the localization

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

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

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

284 Cultures of rabbit synovial fibroblasts were exposed to these vectors and s

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.