ライフサイエンスコーパス: MCP-1

1 MCP-1 and IL-7 concentrations increased after lymphodepl

2 MCP-1 antibody significantly decreased tumor burden and

3 MCP-1 induces a dose-responsive increase in Nf1(+/-) mac

4 MCP-1 inhibition resulted in reduced CCR2-expressing Ly6

5 MCP-1 inhibition, however, increased glomerular endothel

6 MCP-1 protein stimulates EC proliferation and migration

7 MCP-1 regulates inflammatory cell recruitment and differ

8 MCP-1-induced monocyte chemotaxis is a crucial event in

9 MCP-1-induced protein-1 (MCPIP1), a critical regulator o

10 IL-8/CXCL8 (P<0.001), IP-10/CXCL10 (P<0.05), MCP-1/CCL2 (P<0.05), macrophage inflammatory protein (MI

11 egulation of monocyte chemotactic protein 1 (MCP-1) and inflammatory cytokine TNF-alpha.

12 response to monocyte chemotactic protein 1 (MCP-1) and lipopolysaccharide compared with WT mouse mac

13 6 (IL-6) and monocyte chemotactic protein 1 (MCP-1) expression were assessed using reverse transcript

14 imulated monocyte chemoattractant protein 1 (MCP-1) from macrophages and possible mechanisms.

15 (VEGF), monocyte chemoattractive protein 1 (MCP-1), and granulocyte colony-stimulating factor (G-CSF

16 ncluding monocyte chemoattractant protein 1 (MCP-1), interleukin (IL) 6, and IL-8.

17 (IP-10), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1 beta (MIP-1bet

18 (G-CSF), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1beta (MIP-1beta

19 such as monocyte chemoattractant protein 1 (MCP-1), TNF-alpha, and IL-6 and hepatic cleaved caspase

20 IL-6 and monocyte chemoattractant protein 1 (MCP-1).

21 -1beta), and monocyte chemotactic protein 1 (MCP-1).

22 (IL-6), and monocyte chemotactic protein 1 (MCP-1).

23 ight and monocyte chemoattractant protein 1 (MCP-1).

24 ction of monocyte chemoattractant protein 1 (MCP-1).

25 p<0.05), monocyte chemoattractant protein-1 (MCP-1) (0.798, p<0.005), transforming growth factor-beta

26 nd decreased monocyte chemotactic protein-1 (MCP-1) (513.3 pg/mL vs 809.5 pg/mL; P = .0.042) concentr

27 factors, monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) secretion from 3T3-L1 ad

28 cytokine monocyte chemoattractant protein-1 (MCP-1) and MCP-1 induced protein-1 (MCPIP1), a suppresso

29 um day 0 monocyte chemoattractant protein-1 (MCP-1) and peak interleukin-7 (IL-7) concentrations abov

30 ation to monocyte chemoattractant protein-1 (MCP-1) as well as IL-17A, which has been linked to cGVHD

31 a), and monocyte chemo attractant protein-1 (MCP-1) in MRSA USA300 skin lesions.

32 imary ligand monocyte chemotactic protein-1 (MCP-1) is critical for monocyte infiltration into the ar

33 report that monocyte chemotactic protein-1 (MCP-1) is secreted by nonpigmented mouse melanocytes by

34 ponectin and monocyte chemotactic protein-1 (MCP-1) levels in culture media were measured by ELISA.

35 /MDC, and monocyte chemoattactant protein-1 (MCP-1) levels were higher in subjects with SAR, whereas

36 S1P and monocyte chemotactic protein-1 (MCP-1) levels were significantly elevated in the broncho

37 ligand, monocyte chemoattractant protein-1 (MCP-1) promotes cancer progression by directly stimulati

38 4 (TLR4) and monocyte chemotactic protein-1 (MCP-1) that colocalize in neurons from the central nucle

39 produced monocyte chemoattractant protein-1 (MCP-1) upon PIM treatment, and absence of DCAR or FcRgam

40 control, and monocyte chemotactic protein-1 (MCP-1) were identified as the most important distinguish

41 nhibition of monocyte chemotactic protein-1 (MCP-1) with the Spiegelmer emapticap pegol (NOX-E36) sho

42 terleukin-6, monocyte chemotactic protein-1 (MCP-1), and soluble CD40 ligand were also observed in th

43 (IP-10), monocyte chemoattractant protein-1 (MCP-1), IFN-gamma, interleukin (IL)-6, IL-8 and IL-1ra (

44 emokine, monocyte chemoattractant protein-1 (MCP-1), is a mediator of PTH's anabolic effects on bone.

45 hemokine Monocyte Chemoattractant Protein-1 (MCP-1)/CCL2 with different binding affinities.

46 N-gamma, monocyte chemoattractant protein 1 [MCP-1; chemokine (C-C motif) ligand 2 (CCL2)], and tumor

47 ], IL-8, monocyte chemoattractant protein 1 [MCP-1], and IL-1beta) than do UN individuals.

48 ined by increased renal expression of LLT-1, MCP-1, and VLA-4.

49 (RANTES, monocyte chemoattractant protein 1[MCP-1], and IP-10) were increased.

50 2, IFN-gamma, and chemokines (IP-10/CXCL-10, MCP-1/CCL-2, MIP-1alpha/CCL-3, RANTES/CCL-5, and interle

51 flammatory proteins, including; IL-6, IL-10, MCP-1, sVCAM-1, MIP-1alpha, IP-10, GM-CSF, M-CSF, TNF-al

52 reduced milk levels of the chemokines IP-10, MCP-1, MCP-3, MCP-5 and MIP-1beta, which in turn augment

53 -12/IL-23p40, IL-12p70, IL-13, IL-16, IP-10, MCP-1, MCP-4, MDC, MIP-1a, TARC, TNFB) was associated wi

54 Mean IP-10, MCP-1, MIP-1beta, and IL-18 levels all decline on therap

55 ls of eotaxin, IFN-gamma, IL-6, IL-8, IL-16, MCP-1, MIF and MIP-1 beta were significantly higher in a

56 flammatory cytokines (IL-1beta, IL-6, IL-17, MCP-1, MIP-1alpha, MIP-2, RANTES, and TNF-alpha), inflam

57 The plasma levels of IL-17A, MCP-1, and monokine induced by IFN-gamma were increased

58 eased the expression of TNF-alpha, IL-1beta, MCP-1, NF-kappaB and caspase activity in control livers

59 significantly decreased TNF-alpha, IL-1beta, MCP-1, NF-kappaB liver expression and caspase 3 activity

60 a, IL-5, IL-6, TNF-alpha, RANTES, MIP-1beta, MCP-1, KC and IL-10).

61 0 (IP-10), CCL22 (MDC), CCL17 (TARC), CCL-2 (MCP-1) and CCL-13 (MCP-4) in both asthma groups after or

62 roinflammatory genes (CXCL1/KC, CXCL2/MIP-2, MCP-1/CCL2, CXCR2, IL-6, ICAM-1, P-selectin, and C5aR) w

63 gher plasma levels of KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-40 were associated with increased

64 her concentrations of KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-40 were each associated with a gre

65 mation, and fibrosis (KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-40).

66 lbumin ratio), and glial activation (YKL-40, MCP-1, and GFAP).

67 e investigated whether plasma KIM-1, YKL-40, MCP-1, suPAR, TNFR-1, and TNFR-2 are associated with GFR

68 the secretion and expression of PAI-1, IL-6, MCP-1 and leptin in mature 3T3-L1 adipocytes under basel

69 educed the expression and secretion of IL-6, MCP-1 and leptin, as well as suppressed the overexpressi

70 PD reduced IL-6, MCP-1, GM-CSF, and IFN-gamma in brains of WT mice and re

71 n of proinflammatory molecules such as IL-6, MCP-1, ICAM-1 and VCAM-1.

72 many pro-inflammatory cytokines (e.g. IL-6, MCP-1, IL-22, TNF-alpha) and pronounced complement consu

73 Levels of IP-10, HGF, IL-6, MCP-1, MIP-1alpha, IL-12p70, IL-18, VEGF-A, PDGF-BB and

74 nflammatory stress response in plasma (IL-8, MCP-1 and CRP collected two hours after temporary separa

75 Production of IL-6, IL-8, MCP-1, and OPG was significantly increased by Poly I:C o

76 IL), cell recruiting (G-CSF, IL-1beta, IL-8, MCP-1, MCP-3, TNF-alpha), polarizing (CXCL13, IL-10, IL-

77 sion of hepatic inflammatory markers (F4/80, MCP-1, TLR4, TLR2 and IL-1beta) and effector caspase (ca

78 tory response, such as CXCL1, CXCL6, PDGF-A, MCP-1 and IL-6.

79 t, and absence of DCAR or FcRgamma abrogated MCP-1 production.

80 romoted bacterial killing but did not affect MCP-1 production.

81 inflammatory cytokine production (TNF-alpha, MCP-1, and KC).

82 inflammatory cytokines (including TNF-alpha, MCP-1, and keratinocyte-derived protein chemokine [KC])

83 regulated the expression of IL-6, TNF-alpha, MCP-1/CCL2 and IFN-gamma in sera, and ameliorated the or

84 monstrated that intravitreal injection of an MCP-1-neutralizing antibody promoted the recovery of ret

85 +/- 5 versus 9 +/- 2 ng/ml, p < 0.0001) and MCP-1 (867 +/- 150 versus 216 +/- 36 ng/ml, p < 0.0001)

86 R2 (0.265, p<0.05), IL-6 (0.129, p<0.05) and MCP-1 (0.779, p<0.05) and lower levels of IL-8 (-1.293,

87 ociated with increased levels of PECAM-1 and MCP-1 in lal(-/-) ECs.

88 nocyte chemoattractant protein-1 (MCP-1) and MCP-1 induced protein-1 (MCPIP1), a suppressor of miR-14

89 lpha, intracellular adhesion molecule 1, and MCP-1; P < 0.05), and reduced oxidative stress, while ma

90 n of the cytokines IL-1beta, IL-8, IL-10 and MCP-1, whereas exposure to platelets from healthy volunt

91 (interleukin-4 [IL-4], IL-6, and IL-10) and MCP-1/CCL2 were detected early after P. yoelii yoelii 17

92 ted A1-KO mice, but levels of KC, IP-10, and MCP-1 were increased.

93 -8, IL-15, IL-16, IL-17, CXCL10 [IP-10], and MCP-1 [CCL2]) in BAL samples (n=233) from patients with

94 mediated production of TNF, IL-6, IL-13, and MCP-1 in a concentration-dependent manner.

95 by their contrasting effects on IL-1beta and MCP-1 production.

96 secretion of VEGF, IL-6, IL-8, IL-1beta and MCP-1, leading to neovascularization and increased resis

97 D11c expression or secretion of IL-1beta and MCP-1.

98 etion of inflammatory mediators IL-1beta and MCP-1.

99 , IL-22, IL-33, IL-17alpha, IL-2, MIP-2, and MCP-1), and neutrophil infiltration (myeloperoxidase sta

100 ration reduced TRAF6 (~20%), CRF (~30%), and MCP-1 (~20%) levels, as well as TLR4 binding to GABA(A)

101 e GRO-alpha (CXCL1), RANTES (CCL5), IL-6 and MCP-1 (CCL2).

102 Vaccination decreased expression of IL-6 and MCP-1 and reduced macrophage infiltration in the aorta.

103 e content, elevated plasma interleukin-6 and MCP-1 levels, and decreased skeletal muscle mass.

104 ignificantly attenuates circulating IL-6 and MCP-1 levels, limits the expression of adhesion molecule

105 Blood levels of IL-6 and MCP-1 remained unchanged, and histology analysis showed

106 active oxygen species and increased IL-6 and MCP-1 secretion in lal(-/-) ECs.

107 ukin (IL)-1-dependent expression of IL-6 and MCP-1, enhances beta-cell apoptosis, and impairs mitocho

108 produced significantly less G-CSF, IL-6, and MCP-1 in the serum, spleen, and liver on day 1 postinfec

109 HFD also increased plasma leptin, IL-6, and MCP-1 in WT and increased arcuate expression of Kiss1 an

110 trophils and serum levels of IL-8, IL-6, and MCP-1 which varied with cause of death.

111 reased serum cytokines (IFN-gamma, IL-6, and MCP-1) and acute toxicity similar to cytokine release sy

112 tory cytokines, such as TNF-alpha, IL-6, and MCP-1.

113 Basal IL-8 and MCP-1 synthesis by monocytes alone did not differ betwee

114 Inhibiting GrmA reduced excessive IL-8 and MCP-1 synthesis in aging to levels similar to younger ad

115 ts, p < 0.05) and governs increased IL-8 and MCP-1 synthesis through TLR4 and caspase-1.

116 ion synergistically triggers IL-6, IL-8, and MCP-1 production, which was not observed for OPG.

117 tus induced the secretion of IL-6, IL-8, and MCP-1, and the upregulation of CD54 (ICAM-1), consistent

118 ion of the CSF biomarkers T-tau, Abeta40 and MCP-1 separates iNPH from cognitive and movement disorde

119 T-tau, Abeta40 and MCP-1 together yielded an area under the curve of 0.86,

120 n algorithm consisting of T-tau, Abeta40 and MCP-1 was designed as a diagnostic tool using CSF biomar

121 eroid treatment, inhibition of TNF-alpha and MCP-1 function or depletion of macrophages suppressed fe

122 lammatory cytokines (including TNF-alpha and MCP-1) in viral-induced exacerbation of asthma and sugge

123 gamma and IL-27, downstream of TNF-alpha and MCP-1, in the mechanism of RSV-induced exacerbation.

124 iated with higher serum IL-6, TNF-alpha, and MCP-1 levels but decreased secretion of IFN-gamma.

125 cirrhosis was associated with higher ATX and MCP-1, female sex with higher ATX and IL-6, older age wi

126 elevated anti-dsDNA, anti-snRNP, CXCL1, and MCP-1 levels compared to untreated mice; however levels

127 hat NFATc4 siRNA reduced CXCL10, CXCL11, and MCP-1 protein levels.

128 Furthermore, levels of VEGF-D and MCP-1 in patient sera correlated positively with each ot

129 of exosomes was abolished when MSC-Exos and MCP-1 were administrated simultaneously.

130 al chemoattractants like chemerin, fMLF, and MCP-1; and doubled the phagocytic activity of these macr

131 on of immune mediators GM-CSF, IFN-gamma and MCP-1, while suppressing an excessive and potentially ha

132 increased production of TNF, IFN-gamma, and MCP-1/CCL2.

133 ulation of macrophages with a CD86(high) and MCP-1(high) M1-like phenotype that suppressed tumor grow

134 lesterol, and increased levels of leptin and MCP-1.

135 VCAM-1 (vascular cell adhesion molecule) and MCP-1 (monocyte chemotactic protein) were reduced in mic

136 , normal T cell expressed and secreted), and MCP-1.

137 cell, with decrease levels of IL-10, TNF and MCP-1.

138 Increased levels of TNFalpha and MCP-1 correlated with IgE-mediated tumor cytotoxicity by

139 Baseline concentrations of VEGF and MCP-1 are associated with anatomic response to anti-VEGF

140 pokines/cytokines including IGF-1, VEGF, and MCP-1, along with decreased AR, Ki67, and microvessel de

141 ntinuously infused female wild-type (WT) and MCP-1(-/-) mice with hPTH or vehicle.

142 vaccine in soluble factors release, such as MCP-1 or IL-15.

143 r (such as YKL-40), or inflammation (such as MCP-1, suPAR, TNF receptor-1 [TNFR-1], and TNFR-2) may i

144 Intravenous PDNF also augments MCP-1 and FKN in TLR signaling-deficient MyD88-knockout

145 d a significant association between baseline MCP-1 levels and higher risk of ischemic stroke (HR, 1.1

146 SAP reduced serum levels of IL-23, IFN-beta, MCP-1, and tumor necrosis factor-alpha, whereas 1866 red

147 ific Src kinase isoform that is activated by MCP-1 and acts upstream of Pyk2 in primary monocytes.

148 ression and secretion of the chemokine CCL2 (MCP-1).

149 ession of AIMP1 (OMIM 603605) (EMAP2), CCL2 (MCP-1) (OMIM +158105), and IL1b (OMIM *147720).

150 d, and massive astroglial induction of CCL2 (MCP-1), a chemokine for CCR2(+) monocytes.

151 L-18, monocyte chemotactic protein-1 (CCL2) (MCP-1), tissue plasminogen activator inhibitor (PAI-1),

152 Moreover, expression of chemokine CCL2, MCP-1 and its receptor CCR2, which play an important rol

153 ithelial growth factor), GM-CSF, IL-10, CCL2/MCP-1, CCL3/MIP-1a, CXCL10/IP-10, CCL5/RANTES, and CCL20

154 ion of COX-2 abrogated the induction of CCL2/MCP-1 expression by beta-adrenergic activation and preve

155 inflammatory state with elevated Ly6C, CCR5, MCP-1 and reduced SR-B1.

156 TNFalpha and the macrophage chemoattractant MCP-1 in lung bronchoalveolar lavage fluid.

157 expression of the proinflammatory chemokine MCP-1.

158 nd in vivo studies identified the chemokines MCP-1, RANTES, and CXCL10 as MAP3K14 targets in tubular

159 ween vCCI and other wild type CC chemokines, MCP-1 (monocyte chemoattractant protein-1), MIP-1beta, a

160 ed associations between baseline circulating MCP-1 levels and risk of any stroke, ischemic stroke, an

161 how 2.3-fold decreased levels of circulating MCP-1.

162 At 30 days after treatment completion, MCP-1 levels remained lower in the experimental group th

163 increase in proinflammatory cytokine (CXCL1, MCP-1, TNF-alpha, and IL-6) expression and infiltration

164 tic factor Bim and proinflammatory cytokines MCP-1, IL-6, and E-selectin.

165 protein 10]), and proinflammatory cytokines (MCP-1 [monocyte chemoattractant protein 1], MIP-1alpha/b

166 rleuckin-6 (r = 0.47; P = .02) and decreased MCP-1 (r = -0.45; P = .03).

167 In order to simultaneously disrupt MCP-1/CCR2 signaling and target CCR2-expressing cancer c

168 erived proteins in combination with elevated MCP-1 compared with HI and the non-iNPH disorders.

169 s article, we show that the endoribonuclease MCP-1-induced protein 1 (MCPIP1; also known as regnase-1

170 uction, and proinflammatory gene expression (MCP-1).

171 al quantities of the proinflammatory factors MCP-1, IL-8, MIP-1alpha, and IL-6, as well as the antiin

172 ken together, this study implicates the FMOD/MCP-1 pathway in the regulation of angiogenesis by local

173 200-fold difference in binding affinity for MCP-1.

174 of the two distinct conformations known for MCP-1 dimers.

175 L7 and the non-cognate ligand CCL2 (formerly MCP-1).

176 BMMs from MCP-1(-/-) mice showed decreased multinucleated osteocla

177 n vitro, bone marrow macrophages (BMMs) from MCP-1(-/-) and WT mice were cultured with M-CSF, RANKL a

178 However, chemokine release (e.g. MCP-1, RANTES and TARC) was significantly reduced in inh

179 Monokine induced by IFN-gamma, MCP-1, and IFN-gamma production induced in T. cruzi-infe

180 ranulocyte colony-stimulating factor (GCSF), MCP-1, tumor necrosis factor alpha (TNF-alpha), and IgG

181 sex, race, and vascular risk factors, higher MCP-1 levels were associated with increased risk of any

182 Human MCP-1-induced protein 1 (MCPIP1, also known as ZC3H12A a

183 These studies identify MCP-1 as a potent chemokine for Nf1(+/-) monocytes/macro

184 esses the TLR9 (toll-like receptor 9), IFNG, MCP-1 (monocyte chemoattractant protein-1) and GM-CSF ge

185 L-4, 5, 10, 13, 17 A, Eotaxin, GM-CSF, IFNy, MCP-1, TARC, TNFalpha, Total IgE, and Endotoxin) were qu

186 e of multiple cytokines including IL6, IL17, MCP-1, and GM-CSF in the tumor-bearing host, and persist

187 ased eNOS expression and caused no change in MCP-1 expression, which was accompanied by reduced macro

188 mice results in a dose-dependent increase in MCP-1 and FKN in the heart and liver with pulse-like kin

189 om homozygous carriers showed an increase in MCP-1 release in carriers of the minor allele, with the

190 HMGB1, and inflammatory mediators, including MCP-1 and TNFalpha.

191 various pro-inflammatory molecules including MCP-1 and IP-10.

192 tly elevated inflammatory markers including: MCP-1 SDF-1a, IL-Ra, MIP-1b, IL-8, and VEGF in compariso

193 hough single PDNF injections do not increase MCP-1 and FKN receptors, multiple PDNF injections at sho

194 imicrobial peptide expression, and increased MCP-1/CCL2 secretion.

195 r GRP78 or linoleic acid treatment increased MCP-1 serum levels, decreased CD47 expression, and incre

196 ionine-beta-synthase pathway, with increased MCP-1 protein and mRNA expression in both THP-1 cells an

197 hat an inflammatory response with increasing MCP-1 and KIM-1 levels precedes loss of renal function.

198 GM-CSF-induced MCP-1/CCR2 signaling plays an important role in the cros

199 f C. albicans repressed F. nucleatum-induced MCP-1 and TNFalpha production in macrophages.

200 upregulating TNFalpha, which in turn induced MCP-1 production by monocytes and tumor cells to promote

201 s also associated with reduced inflammation (MCP-1, MIP-2, TNF-alpha, IL-6 and CD68), decreased accum

202 metastasis at least partially by inhibiting MCP-1 secretion from adipocytes independent of direct ef

203 xpressed the proinflammatory mediators iNOS, MCP-1 and IL-1beta.

204 tokines (IL-1beta, IL-6) and chemokines (KC, MCP-1) known to drive tissue damage.

205 Plasma leukocyte chemokines (KC, MCP-1, and RANTES) and myeloperoxidase activity were als

206 ressing cancer cells for drug delivery, KLAK-MCP-1 micelles consisting of a CCR2-targeting peptide se

207 In vitro, KLAK-MCP-1 micelles were observed to bind and induce cytotoxi

208 In vivo, KLAK-MCP-1 micelles inhibited tumor growth (34 +/- 11%) in a

209 n the two cell types showed that the ligand (MCP-1) is more highly expressed in KCs than in RHMs, whe

210 d the expression of THP-1-derived macrophage MCP-1 by enhancing NF-kappaB p65 phosphorylation, nuclea

211 sulted in a reduced THP-1-derived macrophage MCP-1 generation.

212 d the expression of THP-1-derived macrophage MCP-1.

213 We report that in murine macrophages MCP-1-induced protein (MCPIP), induced by KLF4, inhibits

214 ased expression of proinflammatory mediators MCP-1 and nuclear factor-kappaB.

215 luding the expression of TGF-beta, NFkappaB, MCP-1, IL-1, IL-6, ICAM-1, VCAM-1 and CD68 macrophages.

216 nary biomarkers including ATP, ACh, nitrite, MCP-1 and IL-5 and participants' confounders, age and ge

217 Notably, MCP-1(-/-) mice were protected against PTH-induced corti

218 intracellular calcium, and the production of MCP 1 (CCL-2) in murine bone marrow-derived MCs.

219 The expression of ICAM-1, VCAM-1 and of MCP-1 was elevated and apoptosis was increased.

220 nse elicited by IL-4, sequential delivery of MCP-1/IL-4 and coating components was distinct in young

221 ved in aged mice, the sequential delivery of MCP-1/IL-4 was capable of restoring both recruitment and

222 Downregulation of MCP-1/CCL2 release was also observed during OASL knock d

223 ssociated with increased renal expression of MCP-1 (monocyte chemoattractant protein-1) and VLA-4 (ve

224 ystathionine could inhibit the expression of MCP-1 in THP-1-derived macrophages induced by ox-LDL via

225 High or low expression of MCP-1, eotaxin, and IL-8 discriminates between eosinophi

226 The presence of high or low expression of MCP-1, eotaxin, and IL-8 identified two separate blood e

227 ha receptor signaling abrogated induction of MCP-1, implicating it in the antitumor effects of IgE.

228 n podocytes in vitro led to an inhibition of MCP-1 and IL-6 expression in response to TNF-alpha and I

229 Conclusions: Higher circulating levels of MCP-1 are associated with increased long-term risk of st

230 : To determine whether circulating levels of MCP-1 are associated with risk of incident stroke in the

231 aucasians have 2-fold higher serum levels of MCP-1 than African Americans.

232 cided with altered mRNA transcript levels of MCP-1, Cx43 and TGFbeta.

233 Loss of MCP-1 or CCR2 expression effectively inhibited Nf1(+/-)

234 Conversely, augmented production of MCP-1 and IL-6 was observed in the glomeruli of C/EBP-al

235 Acute-phase production of MCP-1 correlated with viremia at 3 months postinfection

236 among individuals in the upper quartiles of MCP-1 levels as compared with the first quartile (HRs, s

237 injury partially through down-regulation of MCP-1.

238 ease of adiponectin and inhibited release of MCP-1 from the fat.

239 nd Mendelian randomization suggest a role of MCP-1 (monocyte chemoattractant protein-1) in atheroscle

240 thy volunteers only induced the secretion of MCP-1.

241 ion, Th2 skewing, and increased secretion of MCP-1.

242 Together this suggests a novel target of MCP-1/CCR-2 axis that could benefit ovarian cancer patie

243 lavages as well as impaired upregulation of MCP-1/CCL2.

244 c studies determine that FMOD is upstream of MCP-1 and promotes its secretion from both melanocytes a

245 induce TNF-alpha, IL-1beta, IL-6, IL-12, or MCP-1 production in STING(-/-) mice.

246 2, but did not affect levels of TNF-alpha or MCP-1.

247 of pulmonary macrophage by TNF-alpha and/or MCP-1 in the mechanisms of RSV-induced exacerbation.

248 pulmonary macrophages with TNF-alpha and/or MCP-1 induced expression of both IFN-gamma and IL-27.

249 mice were cultured with M-CSF, RANKL and/or MCP-1.

250 mice did not show elevated levels of S1P or MCP-1.

251 for scrambled siRNA did not inhibit TLR4 or MCP-1 expression nor reduce binge drinking, identifying

252 Infusion of amplicons for TLR4 or MCP-1 siRNA into the CeA or VTA from the P rats inhibite

253 some cytokines (TNF-a, IL-3) but not others (MCP-1, IL-4).

254 Plasma MCP-1, suPAR, and YKL-40 were not independently associat

255 resulted in a significant decrease in plasma MCP-1 on day 3 and reduced exhaled breath condensate aci

256 rophage content within these lesions, plasma MCP-1 levels decreased upon WTD feeding.

257 pression of monocyte chemoattractant protein MCP-1, which in peripheral blood mononuclear cells (PBMC

258 leukin 18, monocyte chemoattractant protein (MCP-1), autotaxin (ATX), and Mac2-binding protein (Mac2B

259 us cytokines such as I-TAC, Eotaxin, RANTES, MCP-1, IFNgamma and MIG demonstrated a biphasic peak tha

260 or LPS - secretory responses (VEGF, RANTES, MCP-1, IL-17A, IFN-gamma, GM-CSF, eotaxin, MIP1-alpha, M

261 had a greater effect on calponin reduction, MCP-1 inhibition, and p38 MAP kinase inhibition than any

262 In vitro, MSC-Exos also down-regulated MCP-1 mRNA expression in primarily cultured retinal cell

263 cascade in primary monocytes that regulates MCP-1-induced monocyte adhesion and migration.

264 Taurocholate induced LPCs to release MCP-1, MIP1alpha, and RANTES into conditioned medium cau

265 nt, sCD14 levels did not change, and sCD163, MCP-1, and IL-6 levels changed at a single time point.

266 nflammatory factors (eg, ICAM-1, E-selectin, MCP-1) in endothelial cells or vascular smooth muscle ce

267 isting of a CCR2-targeting peptide sequence (MCP-1 peptide) and the apoptotic KLAKLAK peptide were sy

268 ntreated mice; however levels of anti-snRNP, MCP-1, and CXCL1 were reduced in pristane-treated Psgl-1

269 duction and exacerbated TNF-alpha-stimulated MCP-1 and IL-8 secretion.

270 r expression of ETS-1 and two ETS-1 targets, MCP-1 and MMP2, did not increase as substantially in ES

271 Taken together, our work demonstrates that MCP-1 has a role in PTH's catabolic effects on bone incl

272 Thus, given that MCP-1 and FKN are chemokines essential to the recruitmen

273 n diabetic nephropathy, we hypothesized that MCP-1 inhibition restores glomerular barrier function th

274 We show that MCP-1 inhibition restores glomerular endothelial glycoca

275 Here, we show that MCP-1 produced by omental adipocytes binding to its cogn

276 We showed that MCP-1 induces Src phosphorylation in a similar time fram

277 netic and experimental evidence suggest that MCP-1 signaling might represent a therapeutic target to

278 Additionally, the MCP-1/CCR2 signaling axis drives the migration of circul

279 In this study, we investigated the MCP-1-mediated activation of Pyk2 (particularly by the p

280 n, nuclear translocation, and binding of the MCP-1 promoter sequence after entry into the nucleus.

281 r U-IRI reveals high-level expression of the MCP-1 receptor Ccr2.

282 A comparison of the MCP-1/C-C chemokine receptor type 2 (CCR2) chemokine sys

283 ylation in a similar time frame and that the MCP-1-induced Pyk2 tyrosine phosphorylation is controlle

284 DNA binding activity, and recruitment to the MCP-1 promoter in ox-LDL-treated macrophages.

285 DNA binding activity, and recruitment to the MCP-1 promoter.

286 and DNA binding level of NF-kappaB with the MCP-1 promoter, which resulted in a reduced THP-1-derive

287 clear translocation and DNA binding with the MCP-1 promoter.

288 ge accumulation and expression of p65, TLR4, MCP-1, and osteopontin.

289 To examine the potential role of a TLR4/MCP-1 signal, we used Herpes Simplex Virus (HSV) vectors

290 binge drinking, identifying a neuronal TLR4/MCP-1 signal that regulates the initiation of voluntary

291 b attenuated the release of IL-6, IL-8, TNF, MCP-1, MIP-1alpha, IFN-gamma, LTB-4, MMP-8 and -9, and I

292 ncluding significant reductions in TNFalpha, MCP-1 (CXCL2), RANTES (CCL5) and KC (CCL5).

293 nocompetent animal, and we identify TNFalpha/MCP-1 signaling as an IgE-mediated mechanism of monocyte

294 ting implants showed a preserved response to MCP-1 in both young and aged animals, restoring delayed

295 k2 activation/phosphorylation in response to MCP-1 stimulation.

296 nsable for monocyte migration in response to MCP-1 stimulation.

297 strate an enhanced proliferative response to MCP-1 when compared with WT SMCs.

298 oke (HR per 1-SD increment in ln-transformed MCP-1, 1.07; 95% CI, 1.01-1.14).

299 response towards an M2-like phenotype, using MCP-1 (macrophage chemotactic protein-1) and IL-4 (inter

300 a, and IL-6 predominated in WT mice, whereas MCP-1 and IL-6 predominated in IRF3-KO mice.