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A genetic polymorphism in the 5' flanking region of the MCP-1 gene is associated with nephritis in lupus through modulating MCP-1 expression. A genetic polymorphism in the 5' flanking region of the MCP-1 gene is associated with nephritis in lupus through modulating MCP-1 expression. A strong upregulation of MCP-1 and RANTES was observed in all the cases, mainly in tubular cells, and there was a strong correlation between the expression of these chemokines and NF-kappaB activation in the same cells. ANF mediates the inhibition of TNF-alpha-induced expression of MCP-1. An increase in MCP-1 may be an important factor in the progression of atherosclerosis in non-diabetic hemodialysis patients. Association between presence of G at position -2518 in MCP-1 promoter region and presence of arthritis in patients with systemic lupus erythematosus. Biologically active MCP-1 secreted into both the uterine lumen and underlying stroma mediates the presence of monocytes, macrophages, and other immune cells in the uterine endometrium. CCL2 may play role in pathobiology of ovarian cancers. CCL2 may represent an autocrine factor important for enhancing HIV-1 virion production likely by affecting the macrophage cytoskeleton. Cerebrospinal fluid MCP-1 activity may be a sensitive marker for neuroinflammation in amyotrophic lateral sclerosis. Circulating ICAM-1, IL-8, and MCP-1 in untreated obstructive sleep apnea were significantly greater than in controls. nCPAP therapy could reduce OSAS-induced hypoxia and generation of inflammatory mediators. Collagen II-reactive T cells in rheumatoid arthritis joints can increase the production of chemokines such as IL-8, MCP-1, and MIP-1 alpha through interaction with synoviocytes. Contact hypersensitivity are significantly enhanced in the hMCP-1 Tgm, which appears to result from a constitutive activation of LC with the systemic presence of large amount of hMCP-1. Data suggest that the A-2518G variant of the SCYA2 has not a major role in the pathogenesis of schizophrenia. Differential production of RANTES and MCP-1 in synovial fluid from the inflamed human knee. Eight tested neuroblastoma cell lines secreted a range of CCL2 (0-21.6 ng/ml. Elevation of MCP-1 in the circulation of peripheral arterial disease(PAD) patients implicates this CC chemokine ligand 2 in inflammatory processes contributing to PAD clinical symptomatology. Escherichia coli activates kidney proximal tubular cells to generate MCP-1 that promotes migration of monocytes in vitro. Estradiol-bound estrogen receptor beta may inhibit MCP-1 gene expression by inhibiting Sp1 and AP-1 transcriptional activities in keratinocytes. Expression in the CNS of transgenic mice is a major pathogenic factor that drives macrophage accumulation in the development of CNS inflammatory disease. Fluid shear stress induces the secretion of monocyte chemoattractant protein-1 in cultured human umbilical vein endothelial cells. HIV-infected patients with the MCP-1-2518G allele have a 5-fold increased risk for atherosclerosis. Human perivascular white adipose tissue has chemotactic properties through the secretion of chemokines. IL-10 has two contrasting actions on MCP-1 production of monocytes/macrophages, between the resting and activated conditions. IL-8 and MCP-1 may contribute to the pathophysiology of adenomyosis. Increased expression in atherectomy specimens from patients with restenosis after percutaneous transluminal coronary angioplasty. Increased expression of monocyte chemotactic protein-1 is associated with invasive ductal breast carcinoma. Induction of the gene encoding macrophage chemoattractant protein 1 by Orientia tsutsugamushi in human endothelial cells involves activation of transcription factor activator protein 1. Inflammatory cytokines mediate C-C (monocyte chemotactic protein 1) and C-X-C (interleukin 8) chemokine expression in human pleural fibroblasts. Inheritance of the -2518 MCP-1 G allele, which appears to affect hepatic MCP-1 expression, may predispose HCV patients to more severe hepatic inflammation and fibrosis. LPS-stimulated production of MCP-1 was significantly less in infected patients. Serum concentrations of both mediators were higher in infected patients and the highest concentrations of MCP-1 were in patients who died. Lack of involvement of polymorphism at position -2518 (A/G) of the MCP-1 gene on the susceptibility to acute allograft rejection among liver transplantation recipients. MCP-1 expression is upregulated in P. gingivalis-infected endothelial cells via reactive oxygen species, p38 MAP kinase, JNK, NF-kappaB, and AP-1. MCP-1 genotype was an independent determinant of plasma MCP-1 level; findings indicate plasma MCP-1 associated with carotid atherosclerosis; -2518 SNP is associated with plasma level of MCP-1, but was not directly associated with carotid atherosclerosis. MCP-1 has an effect on astrocytes that is mediated by caveolin-1. MCP-1 is induced by 13-hydroperoxyoctadecadienoic acid in the vasculature via activation of NF-kappa B. MCP-1 is involved in the regulation of chemotaxis and function of monocytes during and early after the end of cardiopulmonary bypass. MCP-1 is substantially regulated upon monocyte contact with various cell wall components from Gram-positive and Gram-negative bacteria. MCP-1 mRNA levels were increased by 40-fold in left ventricle of myocardial infarction model mice; a transfected N-terminal deletion mutant of the human MCP-1 gene improved the survival rate and symptomology. MCP-1 mainly down-regulates the expression of chemotactic genes influencing neutrophilic granulocyte expression. MCP-1 may play a novel role as a protective agent against the toxic effects of glutamate and HIV-1 tat; neuronal and astrocytic apoptosis in culture was significantly inhibited by co-treatment with MCP-1 or RANTES but not IP-10. MCP-1 may play a role in progression of human esophageal carcinoma through its role in angiogenesis. MCP-1 modulates the differentiation of monocytes into dendritic cells and may thereby inhibit Th1 cell development. MCP-1 polymorphism is slightly associated with the susceptibility to rheumatoid arthritis in patients lacking the HLA shared epitope. MCP-1 produced by human gastric carcinoma cells plays a role in angiogenesis via macrophage recruitment and activation. MCP-1 significantly increased the number of TRAP-positive multinuclear bone-resorbing osteoclasts. MCP-1, MIP-1beta, and IL-8 elevated in relapsing polychondritis(RP) are proinflammatory chemokines, characteristic of activation of monocytes and macrophages and, in the case of IL-8, also of neutrophils. Role for cell-mediated immune response in RP. MCP-1/CCR2 may play a role in Ca2+ influx-dependent TF regulation in the monocyte-endothelial cell interaction in the impairment of nitric oxide synthesis. MCP1 is upregulatied in Peyronie's disease. Monocyte chemoattractant protein-1 induces proliferation and interleukin-6 production in smooth muscle cells by differential activation of nuclear factor-kappa B and activator protein-1. Monocyte chemotactic protein-1 and macrophage migration inhibitory factor production by peritoneal macrophages may contribute to paracrine and autocrine activation and to macrophage accumulation in peritoneal cavity of women with endometriosis. Monocyte chemotactic protein-1 directly induces human vascular smooth muscle proliferation. Myxomas with both high tumor and high stromal MCP-1 expression had a higher macrophage count than other myxomas. In cardiac myxoma, MCP-1 and thymidine phosphorylase may be important angiogenic signals accompanying growth. Oncostatin M induces CCL-2 expression in osteoblasts. Activation of MEK/ERK and STAT pathways, which leads to c-Fos expression and AP-1-DNA binding, is involved in process. Signaling requires tyrosine kinase and protein kinase C but not COX-2. Our aim was to determine whether the MCP-1 -2518 A/G polymorphism affects the severity of acute pancreatitis. Our findings suggest a limited role for CCL2/CCR2 in early active multiple sclerosis. Proapoptotic stimuli upregulate MCP-1 expression by vascular smooth muscle cells through caspase- and calpain-dependent release of interleukin-1alpha. RANTES is more involved than MCP-1 in recruiting inflammatory cells in rhinological disease and may reflect the degree of local inflammation as consequence of the specific chemoattractant properties of RANTES. ROS such as superoxide and H(2)O(2) derived from Rac1-activated NADPH oxidase mediate TNF-alpha-induced MCP-1 expression in endothelial cells. Recipients of renal transplants homozygous for the -2518 G mutation of the MCP-1 gene are at risk for premature kidney graft failure. Results show that high ambient glucose does not affect mesangial monocyte chemoattractant protein-1 release and decreases its chemokine receptor 2 (CCR2) receptor expression. Role in the development of bronchiolitis associated with influenza and RSV infections in infants and children. Role of the MCP-1 promoter -2518 polymorphism in clinical heterogeneity of schizophrenia. Simvastatin reduces expression of the proinflammatory cytokine monocyte chemoattractant protein-1 in circulating monocytes from hypercholesterolemic patients. Single nucleotide polymorphism in this gene supports role for MCP-1 in pathologies associated with hyperinsulinaemia. SphK1 mediates TNF-alpha-induced MCP-1 gene expression through a p38 MAPK-dependent pathway and may participate in oscillatory flow-mediated proinflammatory signaling pathway in the vasculature. The A -2518G polymorphism of the MCP-1 gene appears to affect MCP-1 expression of skin fibroblasts of patients with systemic sclerosis; the G/G genotype may predispose patients. The A-2518G polymorphism in MCP-1 gene does not seem to be a risk factor for the development of AD, but its presence correlates with higher levels of serum MCP-1, which can contribute to increase the inflammatory process occurring in AD. The MCP-1 (-2518) gene polymorphism is unlikely to confer genetic susceptibility to Alzheimer's disease in this large Spanish population. The ability of activated protein C to upregulate the production of MCP-1 is most likely by increasing the stability of MCP-1-mRNA rather than by transcriptional activation via NF-KB. The capacity of in vitro factors to decrease human islet MCP-1 release suggests strategies to increase the success of islet transplantation. The induction of IL-13 and MCP-1 gene expression by IL-1beta was accompanied by the activation of IL-1 receptor-associated kinase and translocation of the transcription factor NF Kappa B into the nucleus. The polymorphisms of the MCP-1 and MIP-1A genes do not play a substantial role in genetic predisposition for sarcoidosis or in clinical manifestations of sarcoidosis in this Japanese population. The present study suggests that the MCP1 promoter -2518 polymorphism may not confer susceptibility to BID itself, but could have an influence on the clinical heterogeneity of BID, at least in the Korean population. The surgical team and the enzyme were independently associated with in vitro CCL2/MCP-1 islet release in islet transplantation. These results indicate that interaction between the Arp2/3 complex and WASP stimulates actin polymerization and integrin beta-1-mediated adhesion during MCP-1-induced chemotaxis of THP-1 cells. These results suggest that hypoxia is an important negative regulator of monocyte chemotaxis to the renal inflamed interstitium, by reducing MCP-1 expression. These studies demonstrate that PEIPC and PECPC isomers are potent activators of endothelial cells increasing synthesis of IL-8 and MCP-1. This gene is one of several cytokine genes clustered on the q-arm of chromosome 17. Cytokines are a family of secreted proteins involved in immunoregulatory and inflammatory processes. The protein encoded by this gene is structurally related to the CXC subfamily of cytokines. Members of this subfamily are characterized by two cysteines separated by a single amino acid. This cytokine displays chemotactic activity for monocytes and basophils but not for neutrophils or eosinophils. It has been implicated in the pathogenesis of diseases characterized by monocytic infiltrates, like psoriasis, rheumatoid arthritis and atherosclerosis. It binds to chemokine receptors CCR2 and CCR4. Toxoplasma gondii tachyzoites induced MCP-1 expression and secretion in infected fibroblasts. Two codons of this human gene suppressed hepatic fibrosis in rats, thus providing feasible gene threapy. Unlike in cells exposed to proinflammatory cytokines, all three MAPKs (ERK, p38 MAPK, and JNK) were required to induce CCL2 secretion in response to activin. Up-regulation of MCP-1 in myeloma cells which express the relevant receptor C-C chemokine receptor 2. We used specific pharmacologic inhibitors to identify the signalling molecules which lead to interleukin (IL)-8 and MCP-1 production in human monocytes in response to M. tuberculosis infection. A marker for acute rejection after liver transplantation. An A/G or G/G genotype may predispose to the development of systemic lupus erythematosus and further indicate that the patients with these genotypes may be at higher risk of developing lupus nephritis. Differential glycosylation allows one to obtain highly effective short-lived CCL2 or less-effective long-lived CCL2 and may thus represent a novel mechanism of adaptation to pathological versus physiological conditions. Enhances the migration of bone marrow stromal cells. Expression induced in macrophages by SARS-CoV infection. Expression of MCP in aiway epithelial cells after injury enhances cell migration and proliferation. Findings suggest that monocyte chemotactic protein-1 (MCP-1) may play a role in preterm labor regardless of the presence of intra-amniotic infection (IAI). First report of monocyte chemotactic protein-1 expression in mesothelial cells induced by oxidized LDL, and provides direct evidence of inflammatory action of peritoneal fluid of women with endometriosis. Homozygosity for G at -2518 in the MCP-1 gene might be a candidate for the genetic marker of Carpal-tunnel syndrome development in Japanese hemodialysis patients. Human monocytes require PKCbeta for the chemotactic response to MCP-1. Increased CXCL10 especially in hypothyroid patients with a more aggressive disorder, and normal CCL2 serum levels in autoimmune thyroiditis. Induction of MCP-1 by Porphyromonas gingivalis in endothelial cells could enhance atherosclerosis progression by contributing to the recruitment of monocytes. Influence of genetic variation in MCP-1 on HIV-1 pathogenesis in large cohorts of HIV-1-infected adults and children. Interacts with the transcriptional repression domain of MBD1. May be a marker of early development of nephropathy in IDDM. Mechanism of gamma-Herpesvirus MCP-1 sequestration. New role of MCP-1 as an arteriogenic factor in hemodialysis patients with cardiovascular disease. No association between the MCP-1 -2518 polymorphism and susceptibility to or clinical disease course in multiple sclerosis. No polymorphic sequence deletion in chronic hepatitis C. Overexpression in mesangial cells by advanced glycation end products. Plasmin induction of MCP-1 in human monocytes. Probiotic E. coli Nissle 1917 specifically upregulates expression of proinflammatory genes and proteins MCP-1, MIP-2alpha, and MIP-2beta in human and mouse intestinal epithelial cells. Results revealed that Porphyromonas gingivalis induces the expression of IL-8 and MCP-1 mRNAs in vascular endothelial cells, but bacterial proteases degrade both chemokines. Results suggest that monocyte chemoattractant protein-1 is produced in renal tubular cells and released into urine in proportion to the degree of proteinuria (albuminuria), and its increased expression in renal tubuli contributes to renal tubular damage. Results therefore identify MCP-1 as a target of the beta-catenin/TCF/LEF pathway in breast tumour cells, a regulation which could play a key role in breast tumour progression. Small inducible cytokine A2 (monocyte chemotactic protein 1, homologous to mouse Sig-je). Some heat-stable component of P. gingivalis, including LPS, may be responsible for the induction of IL-8 and MCP-1 in HUVECs by a CD14-dependent mechanism. Stretching of mesangial cells stimulates their monocyte chemoattractant activity via an NF-kappaB-mediated, MCP-1-dependent pathway. That integrin-mediated cell adhesion to the ECM can induce MCP-1 expression through activation of FAK, and suggest a role for altered extracellular matrix deposition in the progression of glomerular diseases by affecting gene expression. The production of MCP-1 and IL-8 in vascular endothelial cells was induced by mast cell granules and amplified by tryptase. Transcription regulated by Tat and the Smad-3 and-4 transcription factors whose activities are induced by the TGFbeta-1 pathway in human astrocytic cells. Upstream signaling events in platelet-induced NF-kappa B activation that induce secretion of NF-kappa B-regulated chemokine MCP-1.
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