No abstract available.
Chemokine CCL2* ; Humans* ; Monocytes* ; Muscle, Smooth, Vascular*

No abstract available.
Chemokine CCL2* ; Endometriosis* ; Endometrium* ; Female ; Humans ; Monocytes*

OBJECTIVETo investigate the potential association between monocyte chemotactic protein 1(MCP-1)in plasma and acute aortic dissection(AAD).

METHODSA total of 110 patients with Stanford type A AAD who had received emergent surgical treatment in Xiangya hospital from September 2011 to September 2014 were enrolled in as the study group;meanwhile,110 patients with simple hypertension who had received treatment in department of cardiology were chosen as the control group. The plasma level of MCP-1 was measured and then compared between these two groups.

RESULTSThe plasma level of MCP-1 in the study group was(257.79±86.52)pg/ml,which was significantly higher than that in control group [(136.57±48.84)pg/ml](P<0.001).

CONCLUSIONThere may be a correlation between plasma MCP-1 level and AAD.

Aneurysm, Dissecting ; Aortic Aneurysm ; Chemokine CCL2 ; Humans

No abstract available.
Chemokine CCL2* ; Humans* ; Mesangial Cells* ; Monocytes* ; Reactive Oxygen Species*

OBJECT: This study was designed to examine the association between monocyte chemoattractant protein-1 (MCP1) -2518 polymorphism and major depressive disorder (MDD). METHODS: Ninety patients with MDD and 114 healthy controls participated in this study. Genotyping was performed by the polymerase chain reaction-restriction fragment length polymorphism method. RESULTS: Genotype and allele distributions in patients with MDD were significantly different from those of the controls. In particular, subjects with the allele A were found to have an increased risk of MDD. CONCLUSION: The present study suggests that the MCP1 -2518 polymorphism may have a potential role for susceptibility to MDD in the Korean population and thus calls for consecutive studies in order to pile up the data with larger different ethnic background.
Alleles ; Chemokine CCL2 ; Depressive Disorder, Major* ; Genotype ; Humans ; Monocytes*

OBJECTIVETo investigate the effects of C-reactive protein (CRP) on monocytes chemotaxis ability in vitro.

METHODSTranswell chemotaxis assay was used to evaluate the changes of chemotactic ability of THP-1 monocytes in each group treated with CRP in different concentration.

RESULTSCRP increased the number of attracted monocytes in response to MCP-1 (monocyte chemoattractant protein-1). When treated with CRP concentration at 2 microg x mL(-1), the number of chemotactic monocytes increased (P < 0.05). The number of attracted monocytes increased as CRP concentration was elevated (P < 0.05).

CONCLUSIONCRP can increase chemotactic ability of THP-1 monocytes in concentration dependent manner.

C-Reactive Protein ; Chemokine CCL2 ; Chemotaxis ; Humans ; In Vitro Techniques ; Monocytes

OBJECTIVE: Bipolar disorder (BD) is a debilitating psychiatric disease with unknown etiology. Recent studies have shown inflammation as a potential contributing factor of BD pathogenesis. However, potential associations between chemokine and chemokine receptor polymorphisms and BD have been fundamentally understudied. To identify participation of chemokines in BD pathogenesis, we examined genetic variants of several chemokine and chemokine receptor genes. METHODS: The study population comprised 200 patients with BD and 195 age- and sex-matched healthy controls. Genotyping of monocyte chemotactic protein 1 (MCP-1) A2518G, CCR2 V64I, CCR5 Δ32, CCR5 A55029G, stromal cell-derived factor 1 (SDF-1) 3'A, and CXCR4 C138T polymorphisms was performed using polymerase chain reaction and restriction enzyme digestion. RESULTS: We found that CCR5-Δ32 II and CXCR4-C138T C+ genotype frequencies contributed to an increased risk for BD. However, no statistical significance could be obtained with these genotypes after Bonferroni correction. A significant asssociation was only found with MCP-1 GG and G+ genotypes, which were markedly more prevalent in patients with BD and these genotypes seemed to significantly increase the risk for BD even after Bonferroni correction. CONCLUSION: Our findings indicate an association between genetic variants of certain chemokine and chemokine receptor (especially MCP-1) genes and BD. The exact mechanisms by which these variants contribute to BD pathogenesis and their clinical implications need to be further investigated.
Bipolar Disorder* ; Chemokine CCL2 ; Chemokine CXCL12 ; Chemokines ; Digestion ; Genotype ; Humans ; Inflammation ; Polymerase Chain Reaction

OBJECTIVETo investigate the effects of montelukast on atherosclerosis and monocyte chemoattractant protein-1 expression in a hypercholesterolemic rabbit model.

METHODSThirty four male New Zealand white rabbits were randomized into four groups including normal control group (n = 6), placebo group (n = 8), atorvastatin group (1.5 mgxkg(-1)xd(-1), beginning at 8(th) weeks for 4 weeks, n = 10) and montelukast group (1 mgxkg(-1)xd(-1), beginning at 8(th) weeks for 4 weeks, n = 10). Rabbits except those in normal control group were fed a high cholesterol diet for 12 weeks. Serum lipids were measured at 0, 8 and 12 weeks after intervention. The intima/media ratio, percentages of macrophages or smooth muscle cells in intima and the expression of MCP-1 mRNA were examined.

RESULTSAtherosclerosis was evidenced in placebo group and atorvastatin or montelukast treatment significantly reduced neointima (0.32 +/- 0.12 and 0.34 +/- 0.10 vs. 1.12 +/- 0.36, P < 0.05) and macrophage content [(9.8 +/- 4.6)% and (11.2 +/- 3.7)% vs. (34.6 +/- 8.8)%, P < 0.05], increased SMC content [(18.6 +/- 6.9)% and (19.2 +/- 8.6)% vs. (5.2 +/- 2.3)%, P < 0.05] and inhibited expression of MCP-1 mRNA (0.42 +/- 0.08 and 0.40 +/- 0.06 vs. 2.36 +/- 0.48, P < 0.01). Montelukast had similar anti-atherogenetic effects as atorvastatin but had no influence on plasma lipids.

CONCLUSIONSMontelukast could attenuate atherosclerosis in this hypercholesterolemic rabbit model which might be attributed to its anti-inflammatory effects.

Animals ; Atherosclerosis ; metabolism ; Chemokine CCL2 ; metabolism ; Hypercholesterolemia ; Macrophages ; metabolism ; Rabbits ; Tunica Intima

OBJECTIVETo investigate the pathological course in intracranial aneurysms.

METHODSNormal intracranial artery tissue (cortex fistulization) from 1 case, ruptured aneurysms tissuses from 11 cases, unruptured aneurysm tissues from 2 cases were obtained by neurosurgical excision. Routine HE staining was used to observe histological characteristics. In situ hybridization was used to observe the expression of the monocyte chemoattractant protein-1 (MCP-1) mRNA in the walls of the normal artery and aneurysms.

RESULTSBy the HE staining showed that the wall of the ruptured aneurysms (10 cases) and unruptured ones (2 cases) had increased intima and connectivum extima. The fibroblast in the intima was arrayed in the disorder. Monocyte-like cells can be seen in the whole aneurysm wall. In one case aneurysms wall (ruptured) glass-like fiber structure was left over, few cells could be seen. In 9 cases, mural thrombus was found. The thrombus represented with organization. In situ hybridization, MCP-1 mRNA was not detectable in the normal artery. The hybridization signal could be observed in the ruptured aneurysms (10 cases) and unruptured ones (2 cases) often in the intima. MCP-1 mRNA appeared to be expressed by fibroblast cells in its cytoplasm. Monocyte-like cells had little cytoplasm, and the signal was seldom seen. The hybridization signal was discontinuous in the intima, MCP-1 mRNA expressed where fibroblast and monocyte-like cells assembled. One ruptured aneurysm had no signal because there were no cells only glass-like fiber. Mural thrombus showed upregulated hybridization signal in the cytoplasm of fibroblasts, phlogocytes and endotheliocytes of its micrangium.

CONCLUSIONThe pathological representation of the ruptured and unruptured aneurysms and the upregulated expresion of MCP-1 in the aneurysm wall suggest that the development of aneurysm may be a course of chronic inflammation in which main inflammatory cells are monocyte-like cells.

Aneurysm, Ruptured ; Chemokine CCL2 ; Endothelium, Vascular ; Humans ; Intracranial Aneurysm ; RNA, Messenger

The aim of the present study was to investigate the role of chemokine CCL2 in angiogenesis of primary adult rat cardiac microvascular endothelial cells (CMEC). The rat CMECs were isolated and identified through morphology examination and immunostaining with CD31 and factor VIII antibodies. The angiogenesis of CMEC on Matrigel was evaluated at different time points. The expression and secretion of CCL2 during the process of angiogenesis was detected by real-time RT-PCR and ELISA, respectively. The results showed that, the primary rat CMEC was isolated successfully, and the angiogenesis of CMEC was significantly induced after Matrigel treatment for 4 h. The expression of CCL2 and CCR2 were increased during angiogenesis, and the secretion of CCL2 was detected after 2 h of angiogenesis and reached the peak concentration of 1 588.1 pg/mL after 4 h. Either CCL2 blocking antibody or CCR2 antagonist significantly reduced the angiogenesis of CMEC. These results suggest that CCL2 is secreted during the process of angiogenesis of CMEC, and CCL2/CCR2 signaling pathway may play an important role in promoting angiogenesis.
Animals ; Chemokine CCL2 ; Endothelial Cells ; Endothelium, Vascular ; Heart ; Neovascularization, Pathologic ; Rats ; Signal Transduction