ライフサイエンスコーパス: synoviocyte

1 RA and osteoarthritis synovium and cultured synoviocytes.

2 receptor is expressed in the synovium and by synoviocytes.

3 esponsiveness to cells lacking IL-6R such as synoviocytes.

4 protein (SZP) in articular chondrocytes and synoviocytes.

5 as RANTES and IFNbeta protein production in synoviocytes.

6 superficial zone articular chondrocytes and synoviocytes.

7 ed differently in articular chondrocytes and synoviocytes.

8 on in both superficial zone chondrocytes and synoviocytes.

9 expression were markedly lower in MKK3(-/-) synoviocytes.

10 tis, was also able to increase expression in synoviocytes.

11 blining cells rather than the intimal lining synoviocytes.

12 in conditioned media from wild-type cultured synoviocytes.

13 e interactions between endothelial cells and synoviocytes.

14 factor kappa B, and it up-regulates Ang1 in synoviocytes.

15 f angiogenesis between endothelial cells and synoviocytes.

16 mmation and proliferation of fibroblast-like synoviocytes.

17 to a lesser degree, in CD68+ macrophage-like synoviocytes.

18 sion in rheumatoid arthritis fibroblast-like synoviocytes.

19 endent invadosome formation in rat and human synoviocytes.

20 is limited to CD-68-positive macrophage-like synoviocytes.

21 -Jun and induction of c-Jun transcription in synoviocytes.

22 ese ICs mediates, in part, IL-8 induction in synoviocytes.

23 bular heads (gC1q-binding protein) of C1q in synoviocytes.

24 of C1q inhibit IC-mediated IL-8 induction in synoviocytes.

25 e IL-8 mRNA and protein production in normal synoviocytes.

26 genes and the proliferation of inflammatory synoviocytes.

27 ith cDNA from noninflammatory osteoarthritis synoviocytes.

28 re confirmed by in vitro studies of cultured synoviocytes.

29 ic lineage characteristics of intimal lining synoviocytes.

30 COX-2 expression induced by IL-1 beta in RA synoviocytes.

31 arthritis (RA) is activated fibroblast-like synoviocytes.

32 influence growth and survival of rheumatoid synoviocytes.

33 ditional markers implicating fibroblast-like synoviocytes.

34 ury could lead to inflammatory activation of synoviocytes.

35 OA, and RA synovial tissue and in primary RA synoviocytes.

36 expression in both RA synovium and cultured synoviocytes.

37 d selectively induced expression of NR4A2 in synoviocytes.

38 ration between platelets and fibroblast-like synoviocytes.

39 their stimulatory effects on fibroblast-like synoviocytes.

40 7 to type I IFN-regulated gene expression in synoviocytes.

41 of proinflammatory cytokines in the primary synoviocytes.

42 hed the invasive capacity of fibroblast-like synoviocytes.

43 RA synoviocytes aberrantly expressed the stress-inducible M

44 for some T cell costimulatory receptors, but synoviocyte accessory cell function was evident even in

45 investigate the roles of OPN-R and OPN-L in synoviocyte adhesion, which contributes to the formation

46 regulating neutrophil viability and reducing synoviocyte adhesion.

47 to be expressed in surface chondrocytes and synoviocytes after joint cavitation had occurred and rem

48 ival, suggesting that it could contribute to synoviocyte aggressive behavior.

49 Though rheumatoid synoviocytes also express a series of secreted collagena

50 eceptor agonists stimulate PGE2 release from synoviocytes, an effect that is greatly enhanced by IL-1

51 ificant, increase in PG release from resting synoviocytes and a dramatic increase in PG release from

52 for cytokine-induced NF-kappaB activation in synoviocytes and assessed the functional consequences of

53 nexpectedly, plasmid DNA was captured by the synoviocytes and expressed transiently following intraar

54 adherin-11 was identified on fibroblast-like synoviocytes and has been demonstrated to play a central

55 IL-1--induced collagenase gene expression in synoviocytes and in joint arthritis, indicating that JNK

56 IFNbeta on proliferation of fibroblast-like synoviocytes and interleukin-10 synthesis in macrophages

57 Cs can be distinguished from fibroblast-like synoviocytes and primary chondrocytes by their morpholog

58 ession of numerous inflammatory molecules in synoviocytes and protected cells against tumor necrosis

59 Innate immune responses activate synoviocytes and recruit inflammatory cells into the rhe

60 lar basis for IL-1 and IL-6 cross-talk in RA synoviocytes and suggest that, in addition to levels of

61 K) is highly activated in RA fibroblast-like synoviocytes and synovium.

62 pes within the tissue, in particular, type A synoviocytes and vascular endothelium.

63 hich can reinforce the action of crystals on synoviocytes and/or induce chondrocytes to secrete enzym

64 ct with resident joint synovial fibroblasts (synoviocytes) and induce the expression of inflammatory

65 NR4A2 was stably overexpressed in normal synoviocytes, and cell proliferation, survival, anchorag

66 has proinflammatory effects on fibroblasts, synoviocytes, and endothelial cells.

67 ro by incubating the microspheres with human synoviocytes, and in vivo by injection into mouse joints

68 -YF also induced apoptosis in osteoarthritis synoviocytes, and levels of apoptosis were increased by

69 Type B fibroblastic synoviocytes are abundant in inflamed joints of patients

70 Synoviocytes are more sensitive to BMP family members an

71 Immunohistochemistry revealed synoviocytes as a significant source of DcR3 production,

72 an in vitro system to model fibroblast-like synoviocyte behavior and function in organizing the syno

73 OPN-R augmented RA fibroblast-like synoviocyte binding mediated by SVVYGLR binding to alpha

74 out mice to determine the function of JNK in synoviocyte biology and inflammatory arthritis.

75 vial sarcoma does not typically arise from a synoviocyte but instead arises in close proximity to bon

76 tissue-destructive properties of rheumatoid synoviocytes but also controls synoviocyte-initiated ang

77 reased phosphorylation of p38 in WT cultured synoviocytes but that p38 activation, IL-1beta, and IL-6

78 Activin up-regulated SZP accumulation in synoviocytes, but not in chondrocytes.

79 (I-C)-induced type I IFN responses in human synoviocytes by increasing ISRE promoter activity.

80 onstrate an induction of mPGES in rheumatoid synoviocytes by proinflammatory cytokines.

81 lasts, adipocytes, and human fibroblast-like synoviocytes by TGFbeta, IL-1beta, TNFalpha, and IL-6.

82 Cultured RA and type B synoviocytes can perform some of the functions of profes

83 es by limiting inflammation through enhanced synoviocyte cell death, which reduces disease severity,

84 nd that cadherin-11 mediated fibroblast-like synoviocyte cell-to-cell adhesion via formation of adher

85 proliferation is implicated.Proliferation of synoviocytes contributes to joint damage in rheumatoid a

86 r activation of glutamate receptors on human synoviocytes contributes to RA disease pathology.

87 ne whether cell lines derived from RA type B synoviocytes could also serve as accessory cells for T l

88 tant p53 transcripts also were identified in synoviocytes cultured from rheumatoid joints.

89 to rheumatoid arthritis (RA) fibroblast-like synoviocytes cultured in vitro, which could be blocked u

90 and S expression in primary fibroblast-like synoviocyte cultures from RA and OA patients.

91 D2, CD11a/CD18 and MHC class II molecules in synoviocyte-dependent T cell activation.

92 RA patients contained substantial amounts of synoviocyte-derived soluble MICA, which failed to induce

93 Among many other proteins, fibroblast-like synoviocytes dominantly express fibroblast activation pr

94 FKN, which is membrane-anchored on synoviocytes, enhances CD4+ T cell adhesion, provides su

95 Although rheumatoid synoviocytes express a multiplicity of proteolytic enzym

96 ial fibroblasts, cultured RA fibroblast-like synoviocytes expressed higher levels of IL-6, IL-8, and

97 Preculture in IFN gamma augmented synoviocyte expression of major histocompatibility compl

98 Stat3-YF-transduced RA synoviocytes failed to grow in culture, exhibited marked

99 Fibroblast-like synoviocyte (FLS) lines were established from rheumatoid

100 The mechanism of fibroblast-like synoviocyte (FLS) transformation into an inflammatory ph

101 The synovial fibroblast, or fibroblast-like synoviocyte (FLS), has a central role in pannus invasion

102 mponent of the pannus is the fibroblast-like synoviocyte (FLS), whose morphology strikingly resembles

103 Fibroblast-like synoviocyte (FLS)/T cell adhesion was measured by the re

104 arthritis (RA) synovium and fibroblast-like synoviocytes (FLS) and 2) somatic mutations previously i

105 timulate primary cultures of fibroblast-like synoviocytes (FLS) and cell lines transfected with TLR-2

106 tively expressed by cultured fibroblast-like synoviocytes (FLS) and could participate in the pathogen

107 ctively, was investigated on fibroblast-like synoviocytes (FLS) and dermal fibroblasts (DF).

108 lining is a condensation of fibroblast-like synoviocytes (FLS) and macrophages one to three cells th

109 Fibroblast-like synoviocytes (FLS) and T cells can activate each other i

110 Fibroblast-like synoviocytes (FLS) are potentially directly involved in

111 We generated fibroblast-like synoviocytes (FLS) cell lines that were bereft of myelom

112 Rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS) display unique aggressive behavior, i

113 Rheumatoid fibroblast-like synoviocytes (FLS) displayed a unique ability to support

114 nflammatory disease in which fibroblast-like synoviocytes (FLS) exhibit an aggressive phenotype.

115 Because resident fibroblast-like synoviocytes (FLS) express receptors for LTbeta, we exam

116 ed levels in highly invasive fibroblast-like synoviocytes (FLS) from arthritic DA rats and from patie

117 hat poly(I-C) stimulation of fibroblast-like synoviocytes (FLS) from IRF-7(-/-) mice resulted in incr

118 res not only discriminate RA fibroblast-like synoviocytes (FLS) from osteoarthritis FLS, but also dis

119 Fibroblast-like synoviocytes (FLS) from patients with rheumatoid arthrit

120 not understood why cultured fibroblast-like synoviocytes (FLS) from patients with rheumatoid arthrit

121 lytic activity in individual fibroblast-like synoviocytes (FLS) from RA and normal subjects.

122 acellular matrix proteins by fibroblast-like synoviocytes (FLS) from rheumatoid arthritis (RA) patien

123 heir functional relevance in fibroblast-like synoviocytes (FLS) has not been determined.

124 nctional organization within fibroblast-like synoviocytes (FLS) have not been defined.

125 The fibroblast-like synoviocytes (FLS) in the synovial intimal lining of the

126 genes were used to transduce fibroblast-like synoviocytes (FLS) in vitro, and the effects of these ce

127 s (RA), the proliferation of fibroblast-like synoviocytes (FLS) is the cause of chronic inflammation

128 haracterized IKK in cultured fibroblast-like synoviocytes (FLS) isolated from synovium of patients wi

129 Cs (mBMMCs) co-cultured with fibroblast-like synoviocytes (FLS) or mouse 3T3 fibroblasts markedly inc

130 Fibroblast-like synoviocytes (FLS) play a major role in invasive joint d

131 Fibroblast-like synoviocytes (FLS) play important roles in the pathogene

132 ruction mediated by invasive fibroblast-like synoviocytes (FLS) plays a central role in pathogenesis

133 Rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS) produce IL-6 and IL-8, which contribu

134 is of MAP3K mRNA in cultured fibroblast-like synoviocytes (FLS) showed that all of the MAP3Ks examine

135 liferation and activation of fibroblast-like synoviocytes (FLS) through soluble mediators as well as

136 of rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS) to function as antigen-presenting cel

137 identify the contribution of fibroblast-like synoviocytes (FLS) to the perpetuation of synovitis, we

138 alyzed in human synovium and fibroblast-like synoviocytes (FLS) using quantitative polymerase chain r

139 lpha7R in human synovium and fibroblast-like synoviocytes (FLS) was determined using immunohistochemi

140 ial adipose tissue (SAT) and fibroblast-like synoviocytes (FLS) was determined using various techniqu

141 denoviral infection of human fibroblast-like synoviocytes (FLS) was followed by poly(I-C) stimulation

142 p53 expression in cultured fibroblast-like synoviocytes (FLS) was then examined.

143 MMR regulation in arthritis, fibroblast-like synoviocytes (FLS) were isolated from synovial tissues a

144 M-1 in synovial fibroblasts, fibroblast-like synoviocytes (FLS) were isolated from the knee joints of

145 Fibroblast-like synoviocytes (FLS) were prepared from Jnk2(-/-) and wild

146 Cultured fibroblast-like synoviocytes (FLS) were stimulated with interleukin-1 (I

147 (RA) have been identified in fibroblast-like synoviocytes (FLS) with Illumina HumanMethylation450 arr

148 recently been identified on fibroblast-like synoviocytes (FLS), and studies in mice have demonstrate

149 cell suspensions of cultured fibroblast-like synoviocytes (FLS), and synovial tissues were examined b

150 Resident cells, such as fibroblast-like synoviocytes (FLS), play a crucial role in rheumatoid ar

151 H activate ASIC-3 located on fibroblast-like synoviocytes (FLS), which are key cells in the inflammat

152 inase expression in cultured fibroblast-like synoviocytes (FLS).

153 rat knee joints and in human fibroblast-like synoviocytes (FLS).

154 estigated in ST and cultured fibroblast-like synoviocytes (FLS).

155 n were evaluated in human RA fibroblast-like synoviocytes (FLS).

156 d form a complex with JNK in fibroblast-like synoviocytes (FLS).

157 in RA synovium and cultured fibroblast-like synoviocytes (FLS).

158 ) in synovial tissue (ST) or fibroblast-like synoviocytes (FLS).

159 n many cell types, including fibroblast-like synoviocytes (FLS).

160 an synovial intimal resident fibroblast-like synoviocytes (FLS).

161 lta in synovium and cultured fibroblast-like synoviocytes (FLS).

162 nd cyclooxygenases (COXs) in fibroblast-like synoviocytes (FLSCs).

163 sly migrate beneath ordinary fibroblast-like synoviocytes (FLSs) and then experience prolonged surviv

164 ttenuated PDGFR signaling in fibroblast-like synoviocytes (FLSs) and TNF-alpha production in synovial

165 In vitro, primary RA fibroblast-like synoviocytes (FLSs) expressed minimal TSP-1 mRNA levels

166 Fibroblast-like synoviocytes (FLSs) from patients with RA and osteoarthr

167 alloproteinase production by fibroblast-like synoviocytes (FLSs) in patients with rheumatoid arthriti

168 Fibroblast-like synoviocytes (FLSs) of patients with rheumatoid arthriti

169 by which mesenchymal-derived fibroblast-like synoviocytes (FLSs) perpetuate synovial inflammation.

170 resident inflammatory cells, fibroblast-like synoviocytes (FLSs), as a potential source of the rhythm

171 n articular chondrocytes and fibroblast-like synoviocytes (FLSs).

172 ted by a 3-fold increase of PGES activity in synoviocytes following treatment with IL-1beta; this inc

173 ed collagenase production by IL-1-stimulated synoviocytes from 196 +/- 28 ng/ml (mean +/- SEM) to 66

174 To test this hypothesis, cultures of synoviocytes from healthy individuals were treated with

175 ential role of JNK was confirmed in cultured synoviocytes from JNK1 knockout mice and JNK2 knockout m

176 m signalling in murine macrophages and human synoviocytes from patients with RA.

177 Activated lymphocytes and synoviocytes from patients with rheumatoid arthritis exp

178 inducible microsomal PGE synthase (mPGES) in synoviocytes from patients with rheumatoid arthritis, it

179 1 are expressed in secretory fibroblast-like synoviocytes from patients with rheumatoid arthritis, th

180 Synovial tissue and fibroblast-like synoviocytes from RA patients were found to express a hi

181 cell lines during growth in vitro; however, synoviocytes from rheumatoid arthritis (RA) patients sus

182 etect lubricin in synovial fluid or cultured synoviocytes from several patients with frameshift or no

183 us, targeting PI3Kdelta in RA could modulate synoviocyte function via anti-inflammatory and disease-a

184 and IRF7 in poly (I-C)-induced signaling and synoviocyte gene expression.

185 lta inhibition also diminished PDGF-mediated synoviocyte growth and sensitized cells to H(2)O(2)-indu

186 uld be chondroprotective in RA by modulating synoviocyte growth, migration, and invasion.

187 s the proliferation of human fibroblast-like synoviocytes (HFLS-RA), derived from RA patients, with a

188 of B19 did not infect human fibroblast-like synoviocytes (HFLSs), there was a >3-fold increase in sy

189 to identify biological pathways that lead to synoviocyte hyperplasia, the principal pathological feat

190 In in vitro studies using RA fibroblast-like synoviocytes, IFNgamma modulated both IL-1beta- and TNFa

191 pe p53 repressor activity in fibroblast-like synoviocytes; (ii) this repression of hMMP-13 gene expre

192 y, using a three-dimensional fibroblast-like synoviocyte in vitro organ culture system, we provide ev

193 ein (FAP) is overexpressed by fibroblastlike synoviocytes in arthritic joints.

194 into the invasive nature of fibroblast-like synoviocytes in chronic synovitis and rheumatoid arthrit

195 lasts, adipocytes, and human fibroblast-like synoviocytes in response to transforming growth factor b

196 ltured synovial fibroblasts and hyperplastic synoviocytes in the rheumatoid tissue.

197 of activated T lymphocytes, macrophages and synoviocytes in the synovial membrane.

198 inant lubricin inhibited the growth of these synoviocytes in vitro.

199 s, is a potent inducer of aFGF production by synoviocytes in vitro.

200 a dominant promoter site in fibroblast-like synoviocytes, including matrix metalloproteinase (MMP)3,

201 ization inhibited invadosome formation in RA synoviocytes, indicating the presence of an autocrine PD

202 of rheumatoid synoviocytes but also controls synoviocyte-initiated angiogenic responses in vivo.

203 However, the functions of MKK4 and MKK7 in synoviocyte innate immune responses have not been determ

204 components, suggesting that distinct stromal-synoviocyte interactions may be mediated by this phenoty

205 sion was restricted to CD68+ macrophage-like synoviocytes, interdigitating cells, and endothelial cel

206 The mechanisms by which fibroblast-like synoviocyte invade are becoming elucidated, and recent w

207 Targeting synoviocyte IRF3 represents a potential approach to supp

208 Hyperplasia of synoviocytes is found in both rheumatoid arthritis and o

209 uction, mediated by invasive fibroblast-like synoviocytes, is a central feature in the pathogenesis o

210 a cellular assay using SW982 fibroblast-like synoviocytes, it suppressed the release of arachidonic a

211 or 1, and several genes capable of mediating synoviocyte-leukocyte interactions, including vascular c

212 nstitutively overexpressed in the rheumatoid synoviocyte line, including a chemokine, stromal cell-de

213 RA type B synoviocyte lines were potent accessory cells for T cell

214 Cells from RA synoviocyte lines, with or without preculture in interfe

215 buffered saline (PBS; n = 14 rats) and human synoviocyte lubricin (1,600 mug/ml; n = 14 rats) were pe

216 osphate buffered saline (PBS) (n = 9), human synoviocyte lubricin (200 microg/ml; n = 9), rhPRG4 (200

217 Animals with ACLT treated with human synoviocyte lubricin and control animals distributed the

218 Treatment with human synoviocyte lubricin resulted in significantly lower OAR

219 On day 17, urinary CTX-II levels in human synoviocyte lubricin- and human SF lubricin-treated anim

220 fter surgery, urinary CTX-II levels in human synoviocyte lubricin-treated animals were lower than in

221 ression is seen in chondrocytes, followed by synoviocytes, lung, and heart.

222 arthritis, the coordinated expansion of the synoviocyte mass is coupled with a pathologic angiogenic

223 of NMDA and KA glutamate receptors on human synoviocytes may contribute to joint destruction by incr

224 ore, we assessed the role of PI3Kdelta in RA synoviocyte migration and invasion.

225 tes (HFLSs), there was a >3-fold increase in synoviocyte migration that could be blocked by phospholi

226 Herein, we demonstrate that human rheumatoid synoviocytes mobilize the membrane-anchored matrix metal

227 heumatoid arthritis (RA) synovial tissue and synoviocytes, no information is available on the locatio

228 THrP expression was examined in synovium and synoviocytes obtained from patients with RA and osteoart

229 hritis patients, the loss of p53 function in synoviocytes or other cells in the joint because of domi

230 rs from the bipolar shape of fibroblast-like synoviocytes or the spherical configuration of primary h

231 Treatment of fibroblast-like synoviocyte organ cultures with a cadherin-11-Fc fusion

232 sion revealed that cultured RA fibroblastoid synoviocytes overexpress certain proinflammatory genes t

233 cted by interruption of tissue blood flow or synoviocyte oxidative metabolism.

234 family proteins known to be expressed in RA synoviocytes, PI3Kalpha was selectively involved in PDGF

235 hat cadherin-11 expressed in fibroblast-like synoviocytes plays a determining role in establishing th

236 ularly in the CD68-negative, fibroblast-like synoviocyte population.

237 s and a dramatic increase in PG release from synoviocytes prestimulated with recombinant human IL-1al

238 ch of the mesenchymal cells, fibroblast-like synoviocytes, primary chondrocytes, and PCs have the gen

239 endogenous NR4A receptors with shRNA reduced synoviocyte proliferation, migration, and MMP-13 express

240 patients with rheumatoid synovitis, regulate synoviocyte proliferation.

241 rocyte cell lines, primary chondrocytes, and synoviocytes provided expression profiles for the select

242 roles of these enzymes in RA fibroblast-like synoviocytes (RA FLS).

243 rane of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs) isolated from the synovium of pat

244 Neither ATP nor UTP stimulated synoviocyte release of IL-1 as measured by specific ELIS

245 iferase reporter plasmids in fibroblast-like synoviocytes revealed that the induction of hMMP1 promot

246 Ectopic expression of NR4A2 in normal synoviocytes significantly increased proliferation and s

247 Both macrophage- and synoviocyte-specific roles of IRF-7 likely contribute to

248 APCs such as macrophages and fibroblast-like synoviocytes suggest a central role of TSP in the expans

249 Cathepsin S expression in macrophage-like synoviocytes suggests dual activity in antigen presentat

250 was measured by thymidine incorporation, and synoviocyte surface markers were analyzed by flow cytome

251 joints is composed of a condensed network of synoviocytes that form an intact layer via cell-to-cell

252 nd PDGFR-mediated invadosome formation in RA synoviocytes that involves the production of PDGF-B indu

253 o the hyperplastic and invasive phenotype of synoviocytes that leads to cartilage destruction, sugges

254 We demonstrate in rheumatoid fibroblast-like synoviocytes that non-catalytic signaling is associated

255 Fibroblast-like synoviocytes that were grown in three-dimensional matric

256 Altered growth and function of synoviocytes, the intimal cells which line joint cavitie

257 Chondrocytes and synoviocytes, the resident cells of joint capsule, marke

258 In rheumatoid arthritis fibroblast-like synoviocytes these inhibitors block ERK activation, cycl

259 s, can respond to superantigens presented by synoviocytes, this interaction could be important in the

260 rts EGF from a growth/survival factor for RA synoviocytes to a death factor.

261 The response of synoviocytes to BMP was stronger than that of superficia

262 the direct pathway, crystals directly induce synoviocytes to proliferate and produce metalloproteinas

263 nimals in control groups were engrafted with synoviocytes transduced with lacZ and neo marker genes.

264 l transfectants and cultured fibroblast-like synoviocytes treated with a blocking cadherin 11-Fc fusi

265 rtilage extracts and injured fibroblast-like synoviocytes, two major targets of complement deposition

266 analysis of ICBP90 shRNA-treated rheumatoid synoviocytes uncovered a subset of proinflammatory and i

267 oid arthritis (RA) synovial tissue (ST), few synoviocytes undergo apoptosis.

268 bnormal growth and survival properties of RA synoviocytes using retroviral-mediated gene transfer of

269 retion of cathepsin K in primary cultures of synoviocytes was determined by real-time polymerase chai

270 ptosis in Stat3-YF-transduced osteoarthritis synoviocytes was suppressed when Stat1 activity was bloc

271 ing the invasive behavior of fibroblast-like synoviocytes, we generated L cell clones expressing wild

272 Chondrocytes and synoviocytes were isolated from articular cartilage and

273 er RNA levels in synovial tissue and primary synoviocytes were measured by quantitative reverse trans

274 phorylation and IL-6 production by MKK3(-/-) synoviocytes were normal.

275 Fibroblast-like synoviocytes were stimulated with polyinosinic-polycytid

276 Synoviocytes were then treated with either sense or anti

277 To achieve this, primary synoviocytes were transduced in culture with a retrovira

278 Primary TMJ synoviocytes were treated with TNF-alpha or IL-1beta wit

279 Primary cultured endothelial cells and synoviocytes were used to study tumor necrosis factor al

280 for a novel mechanism of IL-8 production by synoviocytes, which could play a key role in inflammatio

281 and IL-1beta stimulated PTHrP expression in synoviocytes, while dexamethasone and interferon-gamma,

282 ry DNA (cDNA) from cultured RA fibroblastoid synoviocytes with cDNA from noninflammatory osteoarthrit

283 r replacement with primitive fibroblast-like synoviocytes with characteristics of immature bone marro

284 We treated early-passage rheumatoid synoviocytes with IL-1 beta and examined the time course

285 Pretreatment of RA synoviocytes with NF-kappa B p65 antisense oligonucleoti

286 eport that cotransfection of fibroblast-like synoviocytes with p53 expression and hMMP13CAT reporter

287 Treatment of synoviocytes with PTHrP(1-34) stimulated IL-6 secretion.