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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
14 nt, participates in such cross-talk for CCL2/monocyte chemotactic protein 1 (MCP-1) production in mas
16 anistic analysis revealed that FAS-regulated monocyte chemotactic protein 1 (MCP-1) secretion by BMMS
17 ll supernatants were assayed for IL-6, IL-8, monocyte chemotactic protein 1 (MCP-1), and FSTL1 by enz
18 nsient depression of interleukin-12 (IL-12), monocyte chemotactic protein 1 (MCP-1), and gamma interf
19 phagocytes, including interleukin-8 (IL-8), monocyte chemotactic protein 1 (MCP-1), and macrophage i
20 duced interleukin-1alpha (IL-1alpha), IL-10, monocyte chemotactic protein 1 (MCP-1), and MCP-3 but no
21 (G-CSF)/keratinocyte-derived chemokine (KC)/monocyte chemotactic protein 1 (MCP-1), and MIP-1alpha f
22 8), interferon-inducible protein 10 (IP-10), monocyte chemotactic protein 1 (MCP-1), and RANTES (regu
23 IP-10), monokine induced by IFN-gamma (MIG), monocyte chemotactic protein 1 (MCP-1), and vascular end
24 efold in the levels of expression of RANTES, monocyte chemotactic protein 1 (MCP-1), gamma-interferon
27 sion of the chemokines interleukin-8 (IL-8), monocyte chemotactic protein 1 (MCP-1), macrophage infla
28 o normal mice, mice genetically deficient in monocyte chemotactic protein 1 (MCP-1), matrix metallopr
29 increased the expression of the CCR2 ligands monocyte chemotactic protein 1 (MCP-1), MCP-3, and MCP-5
36 proteins stromal-derived factor 1 (Sdf1) or monocyte chemotactic protein 1 (Mcp1) enhanced (when sil
37 in turn responded to Reelin by up-regulating monocyte chemotactic protein 1 (MCP1) expression, which
41 e sought to identify the RhoGEFs involved in monocyte chemotactic protein 1 (MCP1)-induced vascular w
43 h plasma levels of interleukin 8 (P = .001), monocyte chemotactic protein 1 (P = .008), and macrophag
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
50 to attract macrophages via the secretion of monocyte chemotactic protein 1 and promote endothelial c
51 reduction in TNF-alpha, IL-1beta, IL-8, and monocyte chemotactic protein 1 concentrations (P < 0.05)
52 except that tumor necrosis factor alpha and monocyte chemotactic protein 1 expression was only eleva
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
68 inhibitory protein (MIP)-1alpha, MIP-1beta, monocyte chemotactic protein 1, and RANTES (regulated up
69 , MIP-2, interferon gamma-inducible protein, monocyte chemotactic protein 1, and T-cell activation ge
70 isregulation of tumor necrosis factor alpha, monocyte chemotactic protein 1, IL-10, transforming grow
71 thelial cells results in increased levels of monocyte chemotactic protein 1, IL-8, and IL-6 cytokines
73 TES, macrophage inflammatory protein 1 beta, monocyte chemotactic protein 1, interleukin-8, and I-309
74 s macrophage inflammatory protein 2 (MIP-2), monocyte chemotactic protein 1, MIP-1beta, inducible pro
75 on IL-12p40, keratinocyte-derived chemokine, monocyte chemotactic protein 1, or macrophage inflammato
76 lammatory protein (MIP)-1alpha , MIP-1beta , monocyte chemotactic protein 1, thymus-and-activation-re
77 genase 1 hypoxia-inducible factor 1 (HIF-1), monocyte chemotactic protein 1, transforming growth fact
80 nd osteoclastogenesis-such as interleukin 6, monocyte-chemotactic protein 1, receptor activator of nu
81 rbitrary units [AU], P = 0.03) and increased monocyte chemotactic protein-1 (3.11 +/- 0.41 nonsmokers
82 +/- 535 vs. 463 +/- 236 pg/mL, p = .02), and monocyte chemotactic protein-1 (7517 +/- 1612 vs. 2983 +
83 ny stimulating factor (GM-CSF), IL-8, IL-18, monocyte chemotactic protein-1 (CCL2) (MCP-1), tissue pl
84 g/mL vs 245.4 pg/mL; P = .012) and decreased monocyte chemotactic protein-1 (MCP-1) (513.3 pg/mL vs 8
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
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
99 acellular adhesion molecule-1 (sICAM-1), and monocyte chemotactic protein-1 (MCP-1) in 2701 participa
100 scular cell adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) in ischemic muscl
102 R2 receptor activation by its primary ligand monocyte chemotactic protein-1 (MCP-1) is critical for m
103 angiogenesis in lighter skin and report that monocyte chemotactic protein-1 (MCP-1) is secreted by no
104 uantified by HPLC/MS/MS, and adiponectin and monocyte chemotactic protein-1 (MCP-1) levels in culture
107 ed levels of Toll-like receptor 4 (TLR4) and monocyte chemotactic protein-1 (MCP-1) that colocalize i
108 he cytokine arrays showed that expression of monocyte chemotactic protein-1 (MCP-1) was profoundly re
112 gy of this process, specifically the role of monocyte chemotactic protein-1 (MCP-1), a cytokine known
113 he production (mRNA and secreted protein) of monocyte chemotactic protein-1 (MCP-1), an adipokine pla
115 scle actin and of the inflammatory mediators monocyte chemotactic protein-1 (MCP-1), macrophage infla
116 ctor-alpha (TNFalpha), interleukin 8 (IL-8), monocyte chemotactic protein-1 (MCP-1), plasminogen acti
117 ein levels of C-C chemokine ligand-2 (CCL-2)/monocyte chemotactic protein-1 (MCP-1), tumor necrosis f
120 ses both amyloid precursor protein (APP) and monocyte chemotactic protein-1 (MCP-1; CCL2 in systemati
121 ding tumor necrosis factor-alpha (TNFalpha), monocyte chemotactic protein-1 (MCP1) and interleukin-1-
124 ule-1 (P < .001), interleukin-10 (P = .041), monocyte chemotactic protein-1 (P = .046), placental gro
125 , but not in pre-bypass or perfusate plasma (monocyte chemotactic protein-1 = 29.5 +/- 2.1 pmoles/l v
126 fidence interval (CI) 1.8-147; p = 0.01] and monocyte chemotactic protein-1 [(MCP-1) 4.8, CI 1.0-23.0
128 nterleukin-1beta [IL-1beta]) and chemokines (monocyte chemotactic protein-1 [MCP-1], IL-8, and macrop
129 suppression of LPS-induced cytokine release (monocyte chemotactic protein-1 [MCP-1], macrophage infla
130 uch as vascular cell adhesion molecule-1 and monocyte chemotactic protein-1 and -3, which function to
131 ncluding mRNA for TNF-alpha, IL-1beta, IL-6, monocyte chemotactic protein-1 and a variety of macropha
132 C expression of adhesion molecules including monocyte chemotactic protein-1 and complement and platel
133 A interference-mediated knockdown assays and monocyte chemotactic protein-1 and intercellular adhesio
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
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-
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
153 macrophages, we showed that mCAT suppressed monocyte chemotactic protein-1 expression by decreasing
154 erleukin (IL)-6, inducible nitric oxide, and monocyte chemotactic protein-1 expression relative to st
156 sion of growth differentiation factor-15 and monocyte chemotactic protein-1 in a murine macrophage ce
158 kin-1beta, tissue necrosis factor-alpha, and monocyte chemotactic protein-1 in the glycogen model and
159 tory function, and increased basal levels of monocyte chemotactic protein-1 in the plasma of LA-apoA-
160 types, but the increase in interleukin-6 and monocyte chemotactic protein-1 levels was less prominent
163 procollagen, smooth muscle alpha-actin, and monocyte chemotactic protein-1 mRNA levels while inducin
166 In contrast to IL-8, CGRP did not induce monocyte chemotactic protein-1 or RANTES synthesis, nor
168 IL-6, vascular endothelial growth factor and monocyte chemotactic protein-1 production and resistance
169 ll as other statins, also reduced RANTES and monocyte chemotactic protein-1 production in mouse endot
170 rosclerotic plaques as well as a decrease in monocyte chemotactic protein-1 production, all of which
172 d interferon-gamma-inducible protein (IP)-10/monocyte chemotactic protein-1 remained depressed, where
173 n contrast, the chemokines interleukin-8 and monocyte chemotactic protein-1 stayed relatively high fr
174 ross endothelial cells expressing VCAM-1 and monocyte chemotactic protein-1 was aberrant compared wit
176 0 is driven by inducible protein-10, whereas monocyte chemotactic protein-1 was central in non-spinal
177 production of interferon-gamma, RANTES, and monocyte chemotactic protein-1 was elevated in TNF KO mi
178 factor-alpha, interleukin (IL)-6, IL-10, and monocyte chemotactic protein-1 were elevated 24 hours af
179 macrophage inflammatory protein-1 alpha and monocyte chemotactic protein-1 were only elevated in tis
180 tion end-products, plasma interleukin-6, and monocyte chemotactic protein-1 were sampled preextracorp
181 expression of chemokines (eg, interleukin-8, monocyte chemotactic protein-1) and other proinflammator
182 chemokine (C-C motif) ligand 2 (CCL2; MCP-1, monocyte chemotactic protein-1) in the glaucoma eye and
183 kines and chemokines (HMGB1, TNFalpha, IL-8, monocyte chemotactic protein-1), and formation of PAI-1/
184 oteins (interferon gamma-induced protein-10, monocyte chemotactic protein-1), and signal transducer a
185 SA-GROalpha-gamma), CCL5 (RANTES), and CCL2 (monocyte chemotactic protein-1), which have been implica
189 y, we hypothesized that the chemokine ligand monocyte chemotactic protein-1, also designated CC chemo
190 locyte macrophage colony-stimulating factor, monocyte chemotactic protein-1, and beta2-microglobulin
191 peptide, vascular endothelial growth factor, monocyte chemotactic protein-1, and blood pressure.
192 ncentrations of IL-12p40, IL-18, RANTES, and monocyte chemotactic protein-1, and elevated production
193 ncluded secretion of interferon-gamma, IL-2, monocyte chemotactic protein-1, and IL-12/IL-23 and prol
194 les, such as platelet-derived growth factor, monocyte chemotactic protein-1, and IL-13, were also red
195 ction of inflammatory proteins (e.g., IL-17, monocyte chemotactic protein-1, and IL-22) in lymphocyte
196 normal t expressed and presumably secreted, monocyte chemotactic protein-1, and interferon-gamma ind
197 or necrosis factor-alpha, interleukin-1beta, monocyte chemotactic protein-1, and macrophage inflammat
198 its target genes such as interleukin-1beta, monocyte chemotactic protein-1, and macrophage inflammat
199 erleukin-8, interferon-inducible protein-10, monocyte chemotactic protein-1, and macrophage inflammat
200 nduced inflammatory mediators, such as IL-6, monocyte chemotactic protein-1, and P-selectin, after re
201 tumor necrosis factor-alpha, interleukin-6, monocyte chemotactic protein-1, and PAE-specific immunog
202 ha, IL-1beta, and IL-6; the chemokines IL-8, monocyte chemotactic protein-1, and RANTES; and the adhe
203 , granulocyte colony-stimulating factor, and monocyte chemotactic protein-1, and reduced granulocyte-
204 , vascular endothelial growth factor, IL-12, monocyte chemotactic protein-1, and S100A8/A9, as well a
205 nnective tissue growth factor, endothelin-1, monocyte chemotactic protein-1, and spermidine/spermine
206 factor, interleukin-6, resistin, leptin, and monocyte chemotactic protein-1, and the upregulation of
207 ase in bronchoalveolar lavage interleukin-6, monocyte chemotactic protein-1, and tumor necrosis facto
208 rations of CD40 antigen, CD40 ligand, IL-16, monocyte chemotactic protein-1, and vascular cell adhesi
209 vation normal T cell expressed and secreted, monocyte chemotactic protein-1, and vascular endothelial
210 increase in plasma markers of inflammation (monocyte chemotactic protein-1, C-reactive protein), the
211 increased circulating TGF-beta1, TGF-beta2, monocyte chemotactic protein-1, C-reactive protein, inte
212 its major ligand, chemokine ligand 2 (CCL2)/monocyte chemotactic protein-1, have been found to influ
213 terleukin-8, interleukin-10, interleukin-18, monocyte chemotactic protein-1, high-mobility group box-
214 primary response gene (88), TLR9, TNF-alpha, monocyte chemotactic protein-1, IFN-gamma inducible prot
215 ed higher concentrations of proinflammatory (monocyte chemotactic protein-1, interleukin [IL]-8, IL-6
216 e Egr-1-regulated proinflammatory chemokines monocyte chemotactic protein-1, KC growth-regulated prot
217 of B6 mice exhibited a dramatic induction of monocyte chemotactic protein-1, macrophage colony-stimul
218 ificantly higher levels of TNF-alpha, IL-10, monocyte chemotactic protein-1, macrophage inflammatory
219 expressed and secreted (RANTES), IP-10, Mig, monocyte chemotactic protein-1, macrophage inflammatory
220 epithelial neutrophil activating protein-78, monocyte chemotactic protein-1, macrophage inflammatory
221 cyte-reactive chemokines examined, including monocyte chemotactic protein-1, macrophage inflammatory
222 s (lipopolysaccharide-induced CXC chemokine, monocyte chemotactic protein-1, macrophage inflammatory
223 cytokine-induced neutrophil chemoattractant, monocyte chemotactic protein-1, macrophage inflammatory
224 significantly lower levels of interleukin-6, monocyte chemotactic protein-1, monocyte chemotactic pro
226 interleukin-6, tumor necrosis factor-alpha, monocyte chemotactic protein-1, P-selectin, and E-select
227 ine, macrophage inflammatory protein-1alpha, monocyte chemotactic protein-1, RANTES, and tumor necros
228 icularly for interleukin IL-1beta, IL-6, and monocyte chemotactic protein-1, relative to stimulation
229 cytokines examined, such as IL-6, IL-10, and monocyte chemotactic protein-1, showed no consistent dif
230 markers, including myeloperoxidase activity, monocyte chemotactic protein-1, tumor necrosis factor-al
231 interleukin-6, tumor necrosis factor-alpha, monocyte chemotactic protein-1, vascular cell adhesion m
232 f the proinflammatory and profibrotic genes (monocyte chemotactic protein-1, vascular endothelial gro
233 es through a porous membrane, in response to monocyte chemotactic protein-1, was blocked when the mem
234 r-alpha, chemokine (C-C motif) ligand 5, and monocyte chemotactic protein-1, when cocultured with tro
236 this study, we report that immune regulator Monocyte chemotactic protein-1-induced protein 1 (MCPIP1
237 -type zinc finger-containing protein MCPIP1 (monocyte chemotactic protein-1-induced protein-1; also k
246 /CXC chemokine ligand 10, interleukin 8, and monocyte chemotactic protein-1/CC chemokine ligand 2.
247 yD88 (MyD88(DN)) decreased the production of monocyte chemotactic protein-1/CCL2 (P=0.000), IL-8/CXCL
248 ctivation (P<0.05) and significantly reduced monocyte chemotactic protein-1/CCL2 (P=0.000), IL-8/CXCL
249 yesian Network suggested that the chemokines monocyte chemotactic protein-1/CCL2 and monokine induced
251 tivity, resulting in decreased expression of monocyte chemotactic protein-1/chemokine (C-C motif) lig
252 leukin-6; macrophage inflammatory protein-2; monocyte chemotactic protein-1; and regulated on activat
253 ocyte chemokine; interleukin-2, -9, and -10; monocyte chemotactic protein-1; leptin; and intracellula
254 ponses were comparable with those induced by monocyte-chemotactic protein-1 (CCL2), but lower than th
257 from controls included interleukin-2 (IL-2), monocyte chemotactic protein 2 (MCP-2), interferon gamma
258 lymphotactin), b) type-2-dominant (eotaxin, monocyte chemotactic protein-2 (MCP-2) and -3 (MCP-3), l
259 macrophage inflammatory protein-1alpha, and monocyte chemotactic protein-2 to mediate phospholipase
261 ein 1beta (MIP-1beta), interleukin 8 (IL-8), monocyte chemotactic protein 3 (MCP-3), IL-2 receptor be
262 ory protein-1alpha (MIP-1alpha), RANTES, and monocyte chemotactic protein-3 (MCP-3) with high affinit
263 11), eotaxin-2 (CCL-24), RANTES (CCL-5), and monocyte chemotactic protein-3 (MCP-3, CCL-7) and 4 (MCP
265 rmal T cell expressed and secreted [RANTES], monocyte chemotactic protein-3 [MCP-3], MCP-4, IL-8, int
266 terleukin-6, monocyte chemotactic protein-1, monocyte chemotactic protein-3, and granulocyte-colony s
268 file characterized by increased nasal lavage monocyte chemotactic protein-3, IFN-alpha2, and plasma I
269 LPS-induced gene expression for induction of monocyte chemotactic protein 5, inducible nitric-oxide s
271 fference in bronchoalveolar lavage levels of monocyte chemotactic protein-5 or interleukin-6 between
272 RNase (mEar) 11, and decreased expression of monocyte chemotactic protein-5, IFN-gamma-inducible prot
274 n some subjects with elevated CSF neopterin, monocyte chemotactic protein/CCL2, and interferon gamma-
275 lpha), MIP-1beta, RANTES, and members of the monocyte chemotactic protein family and is also a recept
277 nregulated expression of the target protein, monocyte chemotactic protein-induced protein 1 (MCPIP1)
278 hat the previously reported immune regulator monocyte chemotactic protein-induced protein 1 (MCPIP1)
283 h recognizes the ligands eotaxin, eotaxin-2, monocyte chemotactic protein (MCP) 3, MCP4, and RANTES,
285 vels of acetylated histone 3 at promoters of monocyte chemotactic protein (MCP)-1 and cytokine-induce
286 -1beta-induced production of IL-6, IL-8, and monocyte chemotactic protein (MCP)-1 and of intercellula
289 ophage inflammatory protein (MIP)-1alpha and monocyte chemotactic protein (MCP)-1 were assessed by EL
290 mRNA for tumor necrosis factor (TNF)-alpha, monocyte chemotactic protein (MCP)-1, and interleukin (I
291 T-cell expressed and secreted (RANTES), CCL2/monocyte chemotactic protein (MCP)-1, CCL3/macrophage in
292 rmal T-cell expressed and secreted (RANTES), monocyte chemotactic protein (MCP)-1, interleukin (IL)-8
293 a, IL-10, tumor necrosis factor (TNF)-alpha, monocyte chemotactic protein (MCP)-1, nuclear factor (NF
294 serum levels of the proatherogenic cytokines monocyte chemotactic protein (MCP)-1, tumor necrosis fac
295 nificant decreases in interleukin (IL)-8 and monocyte chemotactic protein (MCP)-1, whereas roxithromy
297 7, LAMP-1) and increases in the secretion of monocyte chemotactic protein (MCP-1) and interleukin (IL
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