ライフサイエンスコーパス: monocyte chemotactic protein

1 so play a proinflammatory role in activating monocyte chemotactic protein.

2 pression of the chemokines interleukin 8 and monocyte chemotactic protein.

3 ion to inflamed tissues via interaction with monocyte chemotactic proteins.

4 7.5-folds), IL-12 (2.3-folds) and chemokines monocyte chemotactic protein 1 (4.5-folds), MIG (4.4-fol

5 ruitment was associated with upregulation of monocyte chemotactic protein 1 (MCP-1) and inflammatory

6 increased proinflammatory cytokines such as monocyte chemotactic protein 1 (MCP-1) and interleukin 6

7 ice exhibit diminished migratory response to monocyte chemotactic protein 1 (MCP-1) and lipopolysacch

8 after a meal, fructose induced production of monocyte chemotactic protein 1 (MCP-1) and reactive oxyg

9 uM) to phagocytize C. neoformans and produce monocyte chemotactic protein 1 (MCP-1) as a function of

10 e inflammatory protein 1beta (MIP-1beta) and monocyte chemotactic protein 1 (MCP-1) biased the immuni

11 ament fibrocyte (SLF) cell line up-regulates monocyte chemotactic protein 1 (MCP-1) expression after

12 Interleukin-6 (IL-6) and monocyte chemotactic protein 1 (MCP-1) expression were a

13 The early presence of monocyte chemotactic protein 1 (MCP-1) in the CNS provid

14 nt, participates in such cross-talk for CCL2/monocyte chemotactic protein 1 (MCP-1) production in mas

15 lagenase IV (matrix metalloproteinase 9) and monocyte chemotactic protein 1 (MCP-1) promoters up to 1

16 In vitro, several chemokines including monocyte chemotactic protein 1 (MCP-1) protect neurons f

17 anistic analysis revealed that FAS-regulated monocyte chemotactic protein 1 (MCP-1) secretion by BMMS

18 ll supernatants were assayed for IL-6, IL-8, monocyte chemotactic protein 1 (MCP-1), and FSTL1 by enz

19 nsient depression of interleukin-12 (IL-12), monocyte chemotactic protein 1 (MCP-1), and gamma interf

20 phagocytes, including interleukin-8 (IL-8), monocyte chemotactic protein 1 (MCP-1), and macrophage i

21 duced interleukin-1alpha (IL-1alpha), IL-10, monocyte chemotactic protein 1 (MCP-1), and MCP-3 but no

22 (G-CSF)/keratinocyte-derived chemokine (KC)/monocyte chemotactic protein 1 (MCP-1), and MIP-1alpha f

23 8), interferon-inducible protein 10 (IP-10), monocyte chemotactic protein 1 (MCP-1), and RANTES (regu

24 IP-10), monokine induced by IFN-gamma (MIG), monocyte chemotactic protein 1 (MCP-1), and vascular end

25 efold in the levels of expression of RANTES, monocyte chemotactic protein 1 (MCP-1), gamma-interferon

26 The inflammatory biomarkers monocyte chemotactic protein 1 (MCP-1), IL-6, IL-8, vasc

27 Here we report that the CC chemokine, monocyte chemotactic protein 1 (MCP-1), induced chemotax

28 sion of the chemokines interleukin-8 (IL-8), monocyte chemotactic protein 1 (MCP-1), macrophage infla

29 o normal mice, mice genetically deficient in monocyte chemotactic protein 1 (MCP-1), matrix metallopr

30 increased the expression of the CCR2 ligands monocyte chemotactic protein 1 (MCP-1), MCP-3, and MCP-5

31 Chemotactic peptides, such as Monocyte Chemotactic Protein 1 (MCP-1), play a key role

32 n of the chemokines interleukin-8 (IL-8) and monocyte chemotactic protein 1 (MCP-1).

33 ion, which may be regulated by the chemokine monocyte chemotactic protein 1 (MCP-1).

34 alpha (TNF-alpha), interleukin 6 (IL-6), and monocyte chemotactic protein 1 (MCP-1).

35 gelatinase-associated lipocalin (NGAL), and monocyte chemotactic protein 1 (MCP-1).

36 NF-alpha), interleukin 1beta (IL-1beta), and monocyte chemotactic protein 1 (MCP-1).

37 in turn responded to Reelin by up-regulating monocyte chemotactic protein 1 (MCP1) expression, which

38 Monocyte chemotactic protein 1 (MCP1) induced Pak1 phosp

39 Monocyte chemotactic protein 1 (MCP1) stimulates phospho

40 Monocyte chemotactic protein 1 (MCP1) stimulates vascula

41 e sought to identify the RhoGEFs involved in monocyte chemotactic protein 1 (MCP1)-induced vascular w

42 rleukin-8 (IL-8); formyl-Met-Leu-Phe (fMLP); monocyte chemotactic protein 1 (MCP1).

43 h plasma levels of interleukin 8 (P = .001), monocyte chemotactic protein 1 (P = .008), and macrophag

44 e colony-stimulating factor (P = 0.002), and monocyte chemotactic protein 1 (P = 0.007).

45 rferon-inducible protein 10 [IP-10], RANTES, monocyte chemotactic protein 1 [MCP-1], and macrophage i

46 ttractant, IFNgamma-inducible 10-kd protein, monocyte chemotactic protein 1 [MCP-1], and MCP-2) and t

47 e the most abundant, but CC chemokines (CCL2/monocyte chemotactic protein 1 and CCL3/macrophage infla

48 in the mRNA stability of the key chemokines monocyte chemotactic protein 1 and IL-8, an elevation of

49 There was also upregulation of monocyte chemotactic protein 1 and macrophage inflammato

50 to attract macrophages via the secretion of monocyte chemotactic protein 1 and promote endothelial c

51 ANTES, IFN-inducible protein 10 (IP-10), and monocyte chemotactic protein 1 chemokine mRNA were detec

52 reduction in TNF-alpha, IL-1beta, IL-8, and monocyte chemotactic protein 1 concentrations (P < 0.05)

53 matrix metalloproteinase 3, IL-6, IL-8, and monocyte chemotactic protein 1 in RASFs.

54 glia cells expressed IL-6 and the chemokine monocyte chemotactic protein 1 in response to IL-1beta s

55 xplants with antibodies to CCR2 receptor and monocyte chemotactic protein 1 prevented entry of monocy

56 cyclooxygenase 2, as well as proinflammatory monocyte chemotactic protein 1 were decreased in respons

57 s of IL-1RA, IL-6, IL-8, IL-15, eotaxin, and monocyte chemotactic protein 1 were higher in deceased p

58 L-6), macrophage inflammatory protein 2, and monocyte chemotactic protein 1 were immune markers of mo

59 inflammatory gene (toll-like receptor 4 and monocyte chemotactic protein 1) expression, and ceramide

60 hat when an inducer of hyperalgesic priming (monocyte chemotactic protein 1) is administered at the s

61 matory cytokines (IL-6, IL-12, TNFalpha, and monocyte chemotactic protein 1) produced by bone marrow-

62 10 (IFNgamma-inducible 10-kd protein), CCL2 (monocyte chemotactic protein 1), and CCL19 (macrophage i

63 pithelial damage was a localized increase in monocyte chemotactic protein 1, a chemokine known to be

64 creased mRNA and secreted protein levels for monocyte chemotactic protein 1, an effect that could con

65 tinocyte chemoattractant, interleukin 1beta, monocyte chemotactic protein 1, and granulocyte colony-s

66 NF-kappaB, monocyte chemotactic protein 1, and inducible nitric oxi

67 activity and the release of IL-1beta, IL-6, monocyte chemotactic protein 1, and macrophage inflammat

68 increases were observed for IL-1beta, IL-6, monocyte chemotactic protein 1, and MyD88 mRNA.

69 inhibitory protein (MIP)-1alpha, MIP-1beta, monocyte chemotactic protein 1, and RANTES (regulated up

70 , MIP-2, interferon gamma-inducible protein, monocyte chemotactic protein 1, and T-cell activation ge

71 isregulation of tumor necrosis factor alpha, monocyte chemotactic protein 1, IL-10, transforming grow

72 thelial cells results in increased levels of monocyte chemotactic protein 1, IL-8, and IL-6 cytokines

73 Levels of monocyte chemotactic protein 1, interleukin-6 (IL-6), an

74 TES, macrophage inflammatory protein 1 beta, monocyte chemotactic protein 1, interleukin-8, and I-309

75 tumor necrosis factor alpha, interleukin 6, monocyte chemotactic protein 1, macrophage inflammatory

76 s macrophage inflammatory protein 2 (MIP-2), monocyte chemotactic protein 1, MIP-1beta, inducible pro

77 on IL-12p40, keratinocyte-derived chemokine, monocyte chemotactic protein 1, or macrophage inflammato

78 lammatory protein (MIP)-1alpha , MIP-1beta , monocyte chemotactic protein 1, thymus-and-activation-re

79 NTES, and -24.9% (2, -44.8 [P = 0.0656]) for monocyte chemotactic protein 1.

80 lls, possibly via release of IL-6, IL-8, and monocyte chemotactic protein 1.

81 nd osteoclastogenesis-such as interleukin 6, monocyte-chemotactic protein 1, receptor activator of nu

82 rbitrary units [AU], P = 0.03) and increased monocyte chemotactic protein-1 (3.11 +/- 0.41 nonsmokers

83 +/- 535 vs. 463 +/- 236 pg/mL, p = .02), and monocyte chemotactic protein-1 (7517 +/- 1612 vs. 2983 +

84 ny stimulating factor (GM-CSF), IL-8, IL-18, monocyte chemotactic protein-1 (CCL2) (MCP-1), tissue pl

85 ratory disease and the levels of chemokines, monocyte chemotactic protein-1 (MCP-1) and CXCL10, in th

86 recruitment to the vessel wall, mediated by monocyte chemotactic protein-1 (MCP-1) and interleukin-8

87 PC) activate endothelial cells to synthesize monocyte chemotactic protein-1 (MCP-1) and interleukin-8

88 genes involved in atherosclerosis, including monocyte chemotactic protein-1 (MCP-1) and macrophage-co

89 otection assay for intragraft levels of Mig, monocyte chemotactic protein-1 (MCP-1) and regulated on

90 H3, stimulated transcription of the gene for monocyte chemotactic protein-1 (MCP-1) and secretion of

91 inflammatory protein-1alpha (MIP-1alpha) and monocyte chemotactic protein-1 (MCP-1) are abundant in a

92 s had elevated expression of proinflammatory monocyte chemotactic protein-1 (MCP-1) at early time poi

93 Monocyte chemotactic protein-1 (MCP-1) binding to its re

94 d TNFalpha-induced production of eotaxin and monocyte chemotactic protein-1 (MCP-1) but not IL-8.

95 ADMA by high pressure liquid chromatography; monocyte chemotactic protein-1 (MCP-1) by ELISA and NF-K

96 ostate cancer cells produced high amounts of monocyte chemotactic protein-1 (MCP-1) compared with PrE

97 Thrombin-stimulated platelets increased monocyte chemotactic protein-1 (MCP-1) expression by mon

98 The monocyte chemotactic protein-1 (MCP-1) gene is expressed

99 Monocyte chemotactic protein-1 (MCP-1) has been recogniz

100 acellular adhesion molecule-1 (sICAM-1), and monocyte chemotactic protein-1 (MCP-1) in 2701 participa

101 scular cell adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) in ischemic muscl

102 We investigated the potential role of monocyte chemotactic protein-1 (MCP-1) in the pathogenes

103 R2 receptor activation by its primary ligand monocyte chemotactic protein-1 (MCP-1) is critical for m

104 angiogenesis in lighter skin and report that monocyte chemotactic protein-1 (MCP-1) is secreted by no

105 uantified by HPLC/MS/MS, and adiponectin and monocyte chemotactic protein-1 (MCP-1) levels in culture

106 S1P and monocyte chemotactic protein-1 (MCP-1) levels were signi

107 The monocyte chemotactic protein-1 (MCP-1) receptor (MCP-1R)

108 ed levels of Toll-like receptor 4 (TLR4) and monocyte chemotactic protein-1 (MCP-1) that colocalize i

109 he cytokine arrays showed that expression of monocyte chemotactic protein-1 (MCP-1) was profoundly re

110 Monocyte chemotactic protein-1 (MCP-1) was suppressed si

111 Lung function, asthma control, and monocyte chemotactic protein-1 (MCP-1) were identified a

112 Inhibition of monocyte chemotactic protein-1 (MCP-1) with the Spiegelm

113 In these studies, we have found that monocyte chemotactic protein-1 (MCP-1), a CC (beta) chem

114 gy of this process, specifically the role of monocyte chemotactic protein-1 (MCP-1), a cytokine known

115 he production (mRNA and secreted protein) of monocyte chemotactic protein-1 (MCP-1), an adipokine pla

116 Lower levels of interleukin-6, monocyte chemotactic protein-1 (MCP-1), and soluble CD40

117 scle actin and of the inflammatory mediators monocyte chemotactic protein-1 (MCP-1), macrophage infla

118 ctor-alpha (TNFalpha), interleukin 8 (IL-8), monocyte chemotactic protein-1 (MCP-1), plasminogen acti

119 ein levels of C-C chemokine ligand-2 (CCL-2)/monocyte chemotactic protein-1 (MCP-1), tumor necrosis f

120 le-1, vascular cell adhesion molecule-1, and monocyte chemotactic protein-1 (MCP-1).

121 ammatory processes mediated by the chemokine monocyte chemotactic protein-1 (MCP-1/CCL2).

122 ses both amyloid precursor protein (APP) and monocyte chemotactic protein-1 (MCP-1; CCL2 in systemati

123 ding tumor necrosis factor-alpha (TNFalpha), monocyte chemotactic protein-1 (MCP1) and interleukin-1-

124 es stimulation of CCR2 chemokine receptor by monocyte chemotactic protein-1 (MCP1).

125 te-macrophage colony-stimulating factor, and monocyte chemotactic protein-1 (p < .05 for all).

126 , but not in pre-bypass or perfusate plasma (monocyte chemotactic protein-1 = 29.5 +/- 2.1 pmoles/l v

127 fidence interval (CI) 1.8-147; p = 0.01] and monocyte chemotactic protein-1 [(MCP-1) 4.8, CI 1.0-23.0

128 The CC chemokine ligand 2 (CCL2) (JE, monocyte chemotactic protein-1 [MCP-1]) and its CC chemo

129 nterleukin-1beta [IL-1beta]) and chemokines (monocyte chemotactic protein-1 [MCP-1], IL-8, and macrop

130 suppression of LPS-induced cytokine release (monocyte chemotactic protein-1 [MCP-1], macrophage infla

131 uch as vascular cell adhesion molecule-1 and monocyte chemotactic protein-1 and -3, which function to

132 ncluding mRNA for TNF-alpha, IL-1beta, IL-6, monocyte chemotactic protein-1 and a variety of macropha

133 C expression of adhesion molecules including monocyte chemotactic protein-1 and complement and platel

134 and expression of the pro-inflammatory genes monocyte chemotactic protein-1 and interleukin-6.

135 r stress induced p38-dependent expression of monocyte chemotactic protein-1 and interleukin-8 in porc

136 ion in response to proatherogenic cytokines (monocyte chemotactic protein-1 and macrophage colony-sti

137 pancreatic induction of the chemoattractants monocyte chemotactic protein-1 and macrophage inflammato

138 influx was preceded by an acute elevation in monocyte chemotactic protein-1 and macrophage inflammato

139 imulated macrophages secreted the chemokines monocyte chemotactic protein-1 and MIP-1beta in a manner

140 motaxis, concurrently lowering the levels of monocyte chemotactic protein-1 and MIP-1beta.

141 With the exception of low levels of monocyte chemotactic protein-1 and RANTES, culture with

142 macrophages exhibited impaired chemotaxis to monocyte chemotactic protein-1 and showed reduced abilit

143 w and directly recruit MM cells through both monocyte chemotactic protein-1 and stromal cell-derived

144 ecules vascular cell adhesion molecule-1 and monocyte chemotactic protein-1 and the consequential adh

145 PAI-1, the secretion of TNFalpha, IL-8, and monocyte chemotactic protein-1 and the formation of PAI-

146 Monocyte chemotactic protein-1 and transforming growth f

147 the aortic arch, and more abundant mRNA for monocyte chemotactic protein-1 and tumor necrosis factor

148 depended on Gr-1(+) cells, and we implicated monocyte chemotactic protein-1 as a potential mediator.

149 rkers: plasminogen activator inhibitor-1 and monocyte chemotactic protein-1 by 4.5- and 4.0-fold, res

150 ntly lower levels of the chemokines IL-8 and monocyte chemotactic protein-1 compared with mothers of

151 Monocyte chemotactic protein-1 concentrations were decre

152 macrophages, we showed that mCAT suppressed monocyte chemotactic protein-1 expression by decreasing

153 erleukin (IL)-6, inducible nitric oxide, and monocyte chemotactic protein-1 expression relative to st

154 In PARP-1(-/-) macrophages, monocyte chemotactic protein-1 expression was severely i

155 sion of growth differentiation factor-15 and monocyte chemotactic protein-1 in a murine macrophage ce

156 enge had no additional effect on circulating monocyte chemotactic protein-1 in either genotype.

157 kin-1beta, tissue necrosis factor-alpha, and monocyte chemotactic protein-1 in the glycogen model and

158 tory function, and increased basal levels of monocyte chemotactic protein-1 in the plasma of LA-apoA-

159 types, but the increase in interleukin-6 and monocyte chemotactic protein-1 levels was less prominent

160 Unexpectedly, serum monocyte chemotactic protein-1 levels were 8-fold higher

161 ignificantly decreased intragraft RANTES and monocyte chemotactic protein-1 mRNA expression.

162 procollagen, smooth muscle alpha-actin, and monocyte chemotactic protein-1 mRNA levels while inducin

163 ted expression of interleukin-6, VCAM-1, and monocyte chemotactic protein-1 mRNAs.

164 There were no differences in monocyte chemotactic protein-1 or macrophage inflammator

165 In contrast to IL-8, CGRP did not induce monocyte chemotactic protein-1 or RANTES synthesis, nor

166 ssion of the IL-8 gene but not the genes for monocyte chemotactic protein-1 or RANTES.

167 IL-6, vascular endothelial growth factor and monocyte chemotactic protein-1 production and resistance

168 ll as other statins, also reduced RANTES and monocyte chemotactic protein-1 production in mouse endot

169 rosclerotic plaques as well as a decrease in monocyte chemotactic protein-1 production, all of which

170 5(+) monocytes in response to increased lung monocyte chemotactic protein-1 production.

171 d interferon-gamma-inducible protein (IP)-10/monocyte chemotactic protein-1 remained depressed, where

172 n contrast, the chemokines interleukin-8 and monocyte chemotactic protein-1 stayed relatively high fr

173 ross endothelial cells expressing VCAM-1 and monocyte chemotactic protein-1 was aberrant compared wit

174 The decrease in lesional monocyte chemotactic protein-1 was associated with the s

175 0 is driven by inducible protein-10, whereas monocyte chemotactic protein-1 was central in non-spinal

176 production of interferon-gamma, RANTES, and monocyte chemotactic protein-1 was elevated in TNF KO mi

177 factor-alpha, interleukin (IL)-6, IL-10, and monocyte chemotactic protein-1 were elevated 24 hours af

178 macrophage inflammatory protein-1 alpha and monocyte chemotactic protein-1 were only elevated in tis

179 expression of chemokines (eg, interleukin-8, monocyte chemotactic protein-1) and other proinflammator

180 chemokine (C-C motif) ligand 2 (CCL2; MCP-1, monocyte chemotactic protein-1) in the glaucoma eye and

181 kines and chemokines (HMGB1, TNFalpha, IL-8, monocyte chemotactic protein-1), and formation of PAI-1/

182 oteins (interferon gamma-induced protein-10, monocyte chemotactic protein-1), and signal transducer a

183 SA-GROalpha-gamma), CCL5 (RANTES), and CCL2 (monocyte chemotactic protein-1), which have been implica

184 oteins (interferon gamma-induced protein-10, monocyte chemotactic protein-1).

185 crosis factor-alpha; MIP-1alpha/beta; MCP-1 (monocyte chemotactic protein-1); and RANTES.

186 In addition, monocyte chemotactic protein-1, a potent mononuclear cel

187 y, we hypothesized that the chemokine ligand monocyte chemotactic protein-1, also designated CC chemo

188 locyte macrophage colony-stimulating factor, monocyte chemotactic protein-1, and beta2-microglobulin

189 peptide, vascular endothelial growth factor, monocyte chemotactic protein-1, and blood pressure.

190 ncentrations of IL-12p40, IL-18, RANTES, and monocyte chemotactic protein-1, and elevated production

191 ncluded secretion of interferon-gamma, IL-2, monocyte chemotactic protein-1, and IL-12/IL-23 and prol

192 les, such as platelet-derived growth factor, monocyte chemotactic protein-1, and IL-13, were also red

193 ction of inflammatory proteins (e.g., IL-17, monocyte chemotactic protein-1, and IL-22) in lymphocyte

194 normal t expressed and presumably secreted, monocyte chemotactic protein-1, and interferon-gamma ind

195 or necrosis factor-alpha, interleukin-1beta, monocyte chemotactic protein-1, and macrophage inflammat

196 its target genes such as interleukin-1beta, monocyte chemotactic protein-1, and macrophage inflammat

197 erleukin-8, interferon-inducible protein-10, monocyte chemotactic protein-1, and macrophage inflammat

198 nduced inflammatory mediators, such as IL-6, monocyte chemotactic protein-1, and P-selectin, after re

199 tumor necrosis factor-alpha, interleukin-6, monocyte chemotactic protein-1, and PAE-specific immunog

200 ha, IL-1beta, and IL-6; the chemokines IL-8, monocyte chemotactic protein-1, and RANTES; and the adhe

201 , granulocyte colony-stimulating factor, and monocyte chemotactic protein-1, and reduced granulocyte-

202 , vascular endothelial growth factor, IL-12, monocyte chemotactic protein-1, and S100A8/A9, as well a

203 nnective tissue growth factor, endothelin-1, monocyte chemotactic protein-1, and spermidine/spermine

204 factor, interleukin-6, resistin, leptin, and monocyte chemotactic protein-1, and the upregulation of

205 ase in bronchoalveolar lavage interleukin-6, monocyte chemotactic protein-1, and tumor necrosis facto

206 rations of CD40 antigen, CD40 ligand, IL-16, monocyte chemotactic protein-1, and vascular cell adhesi

207 vation normal T cell expressed and secreted, monocyte chemotactic protein-1, and vascular endothelial

208 increase in plasma markers of inflammation (monocyte chemotactic protein-1, C-reactive protein), the

209 increased circulating TGF-beta1, TGF-beta2, monocyte chemotactic protein-1, C-reactive protein, inte

210 its major ligand, chemokine ligand 2 (CCL2)/monocyte chemotactic protein-1, have been found to influ

211 terleukin-8, interleukin-10, interleukin-18, monocyte chemotactic protein-1, high-mobility group box-

212 primary response gene (88), TLR9, TNF-alpha, monocyte chemotactic protein-1, IFN-gamma inducible prot

213 ed higher concentrations of proinflammatory (monocyte chemotactic protein-1, interleukin [IL]-8, IL-6

214 e Egr-1-regulated proinflammatory chemokines monocyte chemotactic protein-1, KC growth-regulated prot

215 of B6 mice exhibited a dramatic induction of monocyte chemotactic protein-1, macrophage colony-stimul

216 s (lipopolysaccharide-induced CXC chemokine, monocyte chemotactic protein-1, macrophage inflammatory

217 ificantly higher levels of TNF-alpha, IL-10, monocyte chemotactic protein-1, macrophage inflammatory

218 expressed and secreted (RANTES), IP-10, Mig, monocyte chemotactic protein-1, macrophage inflammatory

219 epithelial neutrophil activating protein-78, monocyte chemotactic protein-1, macrophage inflammatory

220 cyte-reactive chemokines examined, including monocyte chemotactic protein-1, macrophage inflammatory

221 cytokine-induced neutrophil chemoattractant, monocyte chemotactic protein-1, macrophage inflammatory

222 In mice deficient for monocyte chemotactic protein-1, monocyte-targeted signal

223 interleukin-6, tumor necrosis factor-alpha, monocyte chemotactic protein-1, P-selectin, and E-select

224 ine, macrophage inflammatory protein-1alpha, monocyte chemotactic protein-1, RANTES, and tumor necros

225 icularly for interleukin IL-1beta, IL-6, and monocyte chemotactic protein-1, relative to stimulation

226 markers, including myeloperoxidase activity, monocyte chemotactic protein-1, tumor necrosis factor-al

227 interleukin-6, tumor necrosis factor-alpha, monocyte chemotactic protein-1, vascular cell adhesion m

228 f the proinflammatory and profibrotic genes (monocyte chemotactic protein-1, vascular endothelial gro

229 es through a porous membrane, in response to monocyte chemotactic protein-1, was blocked when the mem

230 r-alpha, chemokine (C-C motif) ligand 5, and monocyte chemotactic protein-1, when cocultured with tro

231 okines RANTES, IFN-inducible protein-10, and monocyte chemotactic protein-1, while LTalphabeta is req

232 oduced by arterial occlusion in wild-type or monocyte chemotactic protein-1-deficient mice.

233 -type zinc finger-containing protein MCPIP1 (monocyte chemotactic protein-1-induced protein-1; also k

234 els of the potent macrophage chemoattractant monocyte chemotactic protein-1.

235 nd MIP-1beta with donor-dependent changes in monocyte chemotactic protein-1.

236 m cytokines, including interleukin-1beta and monocyte chemotactic protein-1.

237 ges also migrated toward galectin-3, but not monocyte chemotactic protein-1.

238 NADPH oxidase (NOX) 2, NOX4, E-selectin, and monocyte chemotactic protein-1.

239 filtration into lesions, and lower levels of monocyte chemotactic protein-1.

240 7,macrophage inflammatory protein-1beta, and monocyte chemotactic protein-1.

241 flammatory protein 2 and KC, and higher lung monocyte chemotactic protein-1.

242 /CXC chemokine ligand 10, interleukin 8, and monocyte chemotactic protein-1/CC chemokine ligand 2.

243 yD88 (MyD88(DN)) decreased the production of monocyte chemotactic protein-1/CCL2 (P=0.000), IL-8/CXCL

244 ctivation (P<0.05) and significantly reduced monocyte chemotactic protein-1/CCL2 (P=0.000), IL-8/CXCL

245 yesian Network suggested that the chemokines monocyte chemotactic protein-1/CCL2 and monokine induced

246 Plasma levels of chemokines (monocyte chemotactic protein-1/CCL2, inducible protein-1

247 tivity, resulting in decreased expression of monocyte chemotactic protein-1/chemokine (C-C motif) lig

248 leukin-6; macrophage inflammatory protein-2; monocyte chemotactic protein-1; and regulated on activat

249 ocyte chemokine; interleukin-2, -9, and -10; monocyte chemotactic protein-1; leptin; and intracellula

250 ponses were comparable with those induced by monocyte-chemotactic protein-1 (CCL2), but lower than th

251 o lymphocyte-attracting chemokines assessed, monocyte-chemotactic protein-1 and macrophage-inflammato

252 ted to play a direct role in angiogenesis is monocyte-chemotactic protein-1.

253 nd KC; IL-4 also increased the production of monocyte-chemotactic protein-1; IL-13 and IL-4 induced e

254 Monocyte chemotactic protein 2 (MCP-2) is a CC chemokine

255 from controls included interleukin-2 (IL-2), monocyte chemotactic protein 2 (MCP-2), interferon gamma

256 lymphotactin), b) type-2-dominant (eotaxin, monocyte chemotactic protein-2 (MCP-2) and -3 (MCP-3), l

257 macrophage inflammatory protein-1alpha, and monocyte chemotactic protein-2 to mediate phospholipase

258 In particular, it was found that the monocyte chemotactic protein 3 (MCP-3) gene expression w

259 ein 1beta (MIP-1beta), interleukin 8 (IL-8), monocyte chemotactic protein 3 (MCP-3), IL-2 receptor be

260 ory protein-1alpha (MIP-1alpha), RANTES, and monocyte chemotactic protein-3 (MCP-3) with high affinit

261 11), eotaxin-2 (CCL-24), RANTES (CCL-5), and monocyte chemotactic protein-3 (MCP-3, CCL-7) and 4 (MCP

262 Monocyte chemotactic protein-3 (MCP-3/CCL7) has potent e

263 rmal T cell expressed and secreted [RANTES], monocyte chemotactic protein-3 [MCP-3], MCP-4, IL-8, int

264 Increased plasma IL-10, monocyte chemotactic protein-3, and IL-6 levels predicte

265 file characterized by increased nasal lavage monocyte chemotactic protein-3, IFN-alpha2, and plasma I

266 LPS-induced gene expression for induction of monocyte chemotactic protein 5, inducible nitric-oxide s

267 Bronchoalveolar lavage fluid levels of monocyte chemotactic protein-5 and interleukin-6 were qu

268 fference in bronchoalveolar lavage levels of monocyte chemotactic protein-5 or interleukin-6 between

269 RNase (mEar) 11, and decreased expression of monocyte chemotactic protein-5, IFN-gamma-inducible prot

270 nd also augmented LTD4-induced production of monocyte chemotactic protein assessed by ELISA.

271 n some subjects with elevated CSF neopterin, monocyte chemotactic protein/CCL2, and interferon gamma-

272 lpha), MIP-1beta, RANTES, and members of the monocyte chemotactic protein family and is also a recept

273 Monocyte chemotactic protein-induced protein 1 (MCPIP1)

274 nregulated expression of the target protein, monocyte chemotactic protein-induced protein 1 (MCPIP1)

275 hat the previously reported immune regulator monocyte chemotactic protein-induced protein 1 (MCPIP1)

276 In this study we investigate how monocyte chemotactic protein-induced protein 1 (MCPIP1;

277 MCPIP1 (monocyte chemotactic protein-induced protein 1) has been

278 MCPIP1 (monocyte chemotactic protein-induced protein 1), a recen

279 MCPIP1 (monocyte chemotactic protein-induced protein 1), also kn

280 h recognizes the ligands eotaxin, eotaxin-2, monocyte chemotactic protein (MCP) 3, MCP4, and RANTES,

281 The reduction in the levels of monocyte chemotactic protein (MCP)-1 and -3 mRNA in HCMV

282 vels of acetylated histone 3 at promoters of monocyte chemotactic protein (MCP)-1 and cytokine-induce

283 -1beta-induced production of IL-6, IL-8, and monocyte chemotactic protein (MCP)-1 and of intercellula

284 protein (MIP)-1alpha, MIP-1beta, MIP-2, and monocyte chemotactic protein (MCP)-1 in both C57BL/6 and

285 Obvious down-regulation of monocyte chemotactic protein (MCP)-1 in the retina was f

286 Monocyte chemotactic protein (MCP)-1 is postulated to pl

287 The specific synthesis of monocyte chemotactic protein (MCP)-1 mRNA by cardiac ven

288 ophage inflammatory protein (MIP)-1alpha and monocyte chemotactic protein (MCP)-1 were assessed by EL

289 mRNA for tumor necrosis factor (TNF)-alpha, monocyte chemotactic protein (MCP)-1, and interleukin (I

290 T-cell expressed and secreted (RANTES), CCL2/monocyte chemotactic protein (MCP)-1, CCL3/macrophage in

291 rmal T-cell expressed and secreted (RANTES), monocyte chemotactic protein (MCP)-1, interleukin (IL)-8

292 a, IL-10, tumor necrosis factor (TNF)-alpha, monocyte chemotactic protein (MCP)-1, nuclear factor (NF

293 serum levels of the proatherogenic cytokines monocyte chemotactic protein (MCP)-1, tumor necrosis fac

294 nificant decreases in interleukin (IL)-8 and monocyte chemotactic protein (MCP)-1, whereas roxithromy

295 Eotaxin, eotaxin-2, monocyte chemotactic protein (MCP)-4, and RANTES induced

296 7, LAMP-1) and increases in the secretion of monocyte chemotactic protein (MCP-1) and interleukin (IL

297 Local expression of chemokine (monocyte chemotactic protein [MCP]-1) and inflammatory c

298 rmal T cell expressed and secreted [RANTES], monocyte chemotactic protein [MCP]-1, macrophage inflamm

299 es, we characterized the effects of IL-13 on monocyte chemotactic proteins (MCPs) and compared the ti

300 (vascular cell adhesion molecule) and MCP-1 (monocyte chemotactic protein) were reduced in mice recei