ライフサイエンスコーパス: MCP-1

1 MCP-1 and CCR2 mRNA, protein, and signaling activity wer

2 MCP-1 exists in equilibrium between monomeric and dimeri

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 protein-1 (MCPIP1), a critical regulator o

9 IP-1alpha, (P < .001), MIP-1beta (P = .005), MCP-1 (P = .03), and TNF-alpha (P = .006).

10 elated with G-CSF (P<0.01), GM-CSF (P<0.01), MCP-1 (P<0.05), MIP-1alpha (P<0.01) and TGF-beta1 (P<0.0

11 antly lower G-CSF (P<0.01), GM-CSF (P<0.01), MCP-1 (P<0.05), MIP-1alpha (P<0.01) and TGF-beta1 (P<0.0

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

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

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

15 6 (IL-6) and monocyte chemotactic protein 1 (MCP-1) expression were assessed using reverse transcript

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

17 Plasma macrophage chemoattractant protein 1 (MCP-1) levels were reduced by FO, but the levels of othe

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

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

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

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

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

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

24 (NGAL), and monocyte chemotactic protein 1 (MCP-1).

25 -1beta), and monocyte chemotactic protein 1 (MCP-1).

26 egulates monocyte chemoattractant protein 1 (MCP-1)/CCL2 and fractalkine (FKN)/CX3CL1 in cellular and

27 culating monocyte chemoattractant protein-1 (MCP-1) and 36% lower lesional vascular cell adhesion mol

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

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

30 mRNA of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha).

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

32 inflammatory monocyte chemotactic protein-1 (MCP-1) at early time points.

33 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) in ischemic muscles, which is required for inflam

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

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

36 Monocyte chemoattractant protein-1 (MCP-1) is involved in the activation and recruitment of

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

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

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

40 4 (TLR4) and monocyte chemotactic protein-1 (MCP-1) that colocalize in neurons from the central nucle

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

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

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

44 analyze monocyte chemoattractant protein-1 (MCP-1), a CC chemokine, and interleukin-8 (IL-8), a CXC

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

46 ssion of monocyte chemoattractant protein-1 (MCP-1), intercellular adhesion molecule 1 (ICAM1), F4/80

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

48 (IP-10), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor alpha (TNF-alpha), and pla

49 MP-1), macrophage chemoattractant protein-1 (MCP-1), vascular cell adhesion molecule-1 (VCAM-1), nucl

50 ecule-1, and monocyte chemotactic protein-1 (MCP-1).

51 ssion of monocyte chemoattractant protein-1 (MCP-1).

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

53 hemokine monocyte chemoattractant protein-1 (MCP-1/CCL2) in response to LPS and thrombin.

54 hemokine monocyte chemoattractant protein-1 (MCP-1/CCL2).

55 -1alpha, monocyte chemoattractant protein 1 [MCP-1], and colony-stimulating factors) responsible for

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

57 = 0.01] and monocyte chemotactic protein-1 [(MCP-1) 4.8, CI 1.0-23.0; p = 0.05].

58 induced monocyte chemoattractant protein -1(MCP-1)/chemokine (C-C motif) ligand 2 (CCL2) expression

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

60 ting factor (M-CSF) ] and chemokines (SDF-1, MCP-1).

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

62 2, IFN-gamma, and chemokines (IP-10/CXCL-10, MCP-1/CCL-2, MIP-1alpha/CCL-3, RANTES/CCL-5, and interle

63 ized levels of IL-6, IL-8, TNF-alpha, IL-10, MCP-1, IL-1ra, G-CSF, and IL-1beta in carriers of TLR5(1

64 cogene (GRO), IL-5, IL-6, IL-7, IL-8, IL-10, MCP-1, MCP-2, MCP-3, and monokine induced by gamma-inter

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

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

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

68 Tumor growth and cytokine responses (IL-1A, MCP-1, TNF-alpha) were observed for two weeks post-impla

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

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

71 0 (IP-10), CCL22 (MDC), CCL17 (TARC), CCL-2 (MCP-1) and CCL-13 (MCP-4) in both asthma groups after or

72 e, 7 markers (IL-6, CD163, IL-10, LBP, IL-2, MCP-1, and IP-10), all with ORs for the 3(rd) versus 1(s

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

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

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

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

77 hepatic inflammatory genes TNF-alpha, IL-6, MCP-1, INF-gamma and NF-kappaB.

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

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

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

81 ids suppressed the upregulation of adipocyte MCP-1 that occurred when adipocytes were cocultured with

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

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

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

85 mobilization of MDSCs in the periphery in an MCP-1-dependent manner and subsequent amelioration of au

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

87 +/- 5 versus 9 +/- 2 ng/ml, p < 0.0001) and MCP-1 (867 +/- 150 versus 216 +/- 36 ng/ml, p < 0.0001)

88 p < 0.04), cholesterol (25%, p < 0.05), and MCP-1 (28%, p = 0.25).

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

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

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

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 roinflammatory cytokines including IL-12 and MCP-1.

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

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

97 despite equivalent levels of KC, MIP-2, and MCP-1 chemokine levels at the wound site.

98 -regulation of IL-6, IL-8, CXCL1, MIP-2, and MCP-1.

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

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

101 ion and suppressed the induction of IL-6 and MCP-1 evoked by LPS and thrombin.

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

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

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

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

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

107 iated inflammatory markers, such as IL-6 and MCP-1.

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

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

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

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

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

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

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

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

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

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

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

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

120 Serum and GCF samples were collected, and MCP-1 levels were estimated using enzyme-linked immunoso

121 Although GM-CSF and MCP-1 cervico-vaginal fluid concentrations were raised,

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

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

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

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

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

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

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

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

130 ne (CXCL13, CCL20, CCL21, eotaxin-2, KC, and MCP-1) production as well as inflammatory cell accumulat

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

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

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

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

135 ophages induced expression of MMPs, VEGF and MCP-1 genes, and increased the invasive potential in A54

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

137 CCL2, also referred to as MCP-1, is critically involved in directing the migration

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

139 w that the Nanobodies directed against CCL2 (MCP-1), CCL5 (RANTES), CXCL11 (I-TAC), and CXCL12 (SDF-1

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

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

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

143 , Ly6G expression, production of serum CCL2 (MCP-1), and susceptibility to C. albicans.

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

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

146 phils, total protein, LDH, CXCL1/KC and CCL2/MCP-1 were also increased (P < 0.01), and so were lung t

147 lactate dehydrogenase (LDH), CXCL1/KC, CCL2/MCP-1 and differential cell counts.

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

149 els of chemokine (C-C motif) ligand 2 (CCL2; MCP-1, monocyte chemotactic protein-1) in the glaucoma e

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

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

152 expression of the proinflammatory chemokine MCP-1.

153 , including interleukin-12 and the chemokine MCP-1, both known to control early parasite replication

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

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

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

157 d GLA-SE transiently upregulated circulating MCP-1, TNFalpha, IFNgamma and IP-10 in blood.

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

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

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

161 e mRNA expression of inflammatory cytokines (MCP-1, IFNgamma, IL-6, IL17F and IL-21) and iii) total (

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

163 beta3-strand) of both monomeric and dimeric MCP-1 but that binding to the dimeric form also influenc

164 e dimerization interface of inactive dimeric MCP-1, thus inducing dissociation to the active monomeri

165 increase was correlated with the diminished MCP-1 and MCP-3 chemokine production and decreased blood

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

167 om I-BOP-treated A549-TPalpha cells enhanced MCP-1-dependent migration of RAW 264.7 macrophages.

168 The survival benefit results from enhanced MCP-1-dependent monocyte recruitment and a subsequent de

169 T cells and elevated levels of the eotaxin, MCP-1, and G-CSF cytokines was observed in the absence o

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 capacity of vascular smooth muscle cells for MCP-1-induced activation of the cyclin D1-CDK6-CDK4-Pak1

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

176 orate, significantly reduced the potency for MCP-1 activation of CCR2.

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

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

179 e reductions in proinflammatory mRNAs (e.g., MCP-1 and TNF-alpha), and improved tissue ATP levels.

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

181 d that the high levels of both serum and GCF MCP-1 found in smokers could explain the severity of per

182 f this study is to analyze the serum and GCF MCP-1 levels of smokers and never-smokers with periodont

183 LR2 pathway intermediates hCXCL8/IL-8, hCCL2/MCP-1, hMMP7, and hTNF-alpha, were also lessened.

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

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

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

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

188 ted a decrease in macrophages, a decrease in MCP-1, and an increase in capillaries, and subjects with

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

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

191 , here we have studied the role of NFATc1 in MCP-1-induced human aortic smooth muscle cell (HASMC) gr

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 line triggered MCP-1 secretion and increased MCP-1-dependent macrophage chemotaxis.

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

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

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

198 nscription factor SP1 mediates I-BOP-induced MCP-1 expression.

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

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

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

205 Mn(2+) also inhibited ROS levels, MCP-1 secretion, and ICAM-1 up-regulation in HUVECs trea

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

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

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

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

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

211 Mean MCP-1 levels in serum and GCF were found to be highest i

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

213 in vivo, whereas the obligate dimeric mutant MCP-1(T10C) was less effective at inducing leukocyte rec

214 The obligate monomeric mutant MCP-1(P8A) was similar to wild type MCP-1 in its ability

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

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

217 g lymph nodes, and in vivo administration of MCP-1 increased the frequency and absolute numbers of MD

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

219 ctrometry (MS/MS) showed that the binding of MCP-1 to a heparin octasaccharide has different dissocia

220 Binding of MCP-1 to heparin octasaccharide isomers of varying sulfa

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

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

223 creases in adipose tissue gene expression of MCP-1 and IL-1beta in the wild-type HFD-fed mice.

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 The induction of MCP-1 was also found in other lung cancer cells H157 and

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

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

230 (P = 0.04), marginally reduced the levels of MCP-1 (P = 0.10), and marginally increased the levels of

231 lcin, IL-10, GM-CSF, and decreased levels of MCP-1 in serum parallel the improvements in bone micro-a

232 pDC-depleted mice showed increased levels of MCP-1 in the draining lymph nodes, and in vivo administr

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

234 rosis was ameliorated with reduced levels of MCP-1, consistent with a profibrotic role for native KIM

235 larized macrophages expressed high levels of MCP-1.

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

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

238 ike) cells, PGE2 inhibited the production of MCP-1 and TNF-alpha while augmenting IL-10 expression.

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

240 EI strongly inhibits the production of MCP-1, a major monocyte chemotactic factor, and either d

241 ed by Abeta-induced microglial production of MCP-1.

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

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

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

245 ed with loss of Treg-mediated suppression of MCP-1.

246 Mechanistically, upregulation of MCP-1 and FKN stems from the interaction of parasite-der

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

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

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

250 2, but did not affect levels of TNF-alpha or MCP-1.

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

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

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

254 nocyte adhesion to HUVECs treated with HG or MCP-1.

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

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

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

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

259 The most potent macrocyclic peptidomimetic (MCP-1), 34, binds to menin with a K(i) value of 4.7 nM a

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

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

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

263 The addition of omega-3 fatty acids reduced MCP-1 expression with no effect on TNF-alpha.

264 rophages, increased capillaries, and reduced MCP-1 expression in insulin-resistant humans and in macr

265 ignificantly reduced GRO, marginally reduced MCP-1, and marginally increased TGF-beta1 from P. gingiv

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

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

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

269 ve-derived norepinephrine directly restrains MCP-1 production by peritoneal macrophages during infect

270 Similarly, MCP-1(P8A) bound more tightly than MCP-1(T10C) to the CC

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

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

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

274 imilarly, MCP-1(P8A) bound more tightly than MCP-1(T10C) to the CCR2-derived sulfopeptides.

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

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

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

278 We show that MCP-1 and IL-8 are physiologically present as a dimer, w

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

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

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

282 We also show that the MCP-1 dimer adopts two conformations, one extended and o

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

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

285 NMR chemical shift mapping using the MCP-1 mutants showed that the sulfated N-terminal region

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 y stimulate invasion of cancer cells through MCP-1-mediated macrophage recruitment.

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

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

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

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 pe (WT) recipients, or WT monocytes given to MCP-1 KO recipients, adipose tissue macrophage (ATM) acc

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

296 o migration of cox-2(-/-) macrophages toward MCP-1, RANTES, MIP-1alpha, or MIP-1beta, as well as cell

297 rtalized proximal tubule cell line triggered MCP-1 secretion and increased MCP-1-dependent macrophage

298 the monomeric and dimeric forms of wild type MCP-1 and shifted the equilibrium to favor the monomeric

299 c mutant MCP-1(P8A) was similar to wild type MCP-1 in its ability to induce leukocyte recruitment in

300 are physiologically present as a dimer, with MCP-1 having two variants of its dimeric form and IL-8 h