OBJECTIVETo investigate the mechanism of monocyte chemoattractant protein-1 (MCP-1) regulations of human gingival fibroblasts (HGF) by challenge of Porphyromonas gingivalis (Pg) with different fimA genotypes.

METHODSPg ATCC 33277 (type I), WCSP115 (type II), WCSP1.5 (type III), W83 (type IV) were assessed for their inductions of MCP-1 expression in HGF. MCP-1 mRNA levels of HGF were determined by real-time RT-PCR and MCP-1 protein levels in culture supernatant by ELISA at different time intervals (1 h, 3h, 6h and 12h) following continuous co-culture of bacteria with HGF.

RESULTSMCP-1 mRNA and protein levels were both up-regulated when HGF co-cultured with different Pg fimA genotypes. Type II was stronger than other fimA genotypes, HGF expressed significantly great amount of MCP-1 mRNA [(25.75 +/- 3.12)-(326.69 +/- 35.35)] and protein [(178.20 +/- 46.20)-(443.46 82.19) ng/L] for different time periods; While Type III was weaker than other fimA genotypes, and the level of MCP-1 mRNA was [ (4.16 +/- 0.82)-(94.17 +/- 18.56)] and protein [(86.95 +/- 23.90)-(264.01 +/- 28.59) ng/L](P < 0.05).

CONCLUSIONSfimA genotypes of Pg are related with the inductions of MCP-1, which might indicate fimA genotype is associated with pathogenesis of Pg.

Cells, Cultured ; Chemokine CCL2 ; metabolism ; Fibroblasts ; metabolism ; Fimbriae Proteins ; genetics ; Genotype ; Gingiva ; cytology ; microbiology ; Humans ; Porphyromonas gingivalis ; genetics

This study was aimed to explore the expression of MIP-1alpha, MCP-1 and their receptors CCR-1, CCR-2 in bcr/abl fusion gene positive CML cells, and to study the effects of P210(bcr/abl) fusion protein tyrosine kinase on expression of MIP-1alpha, MCP-1 and their receptors CCR-1, CCR-2 mRNAs in chronic myeloid leukemia cells. The expression levels of MIP-1alpha, MCP-1 and their receptors CCR-1, CCR-2 mRNA were detected by semi-quantitative RT-PCR in bcr/abl negative cells, bcr/abl positive cells, and P210(bcr/abl)-Rb-C-Box positive cells. The results showed that MIP-1alpha and CCR-1 mRNAs were expressed in bcr/abl negative cells, but not in positive cells. Both MCP-1 and CCR-2 mRNA cannot be detected in both bcr/abl positive and negative cells. After inhibiting P210(bcr/abl) tyrosine kinase activity by Rb-C-Box, expressions of MIP-1alpha and CCR-1 mRNAs were restored to normal (similar to P210(bcr/abl) negative cells). It is concluded that P210(bcr/abl) fusion protein inhibits the expression of MIP-1alpha and CCR-1 in chronic myeloid leukemia cells, but does not inhibit MCP-1 and CCR-2 mRNA expressions in these leukemia cells.
Chemokine CCL2 ; biosynthesis ; genetics ; Chemokine CCL3 ; Chemokine CCL4 ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; metabolism ; Macrophage Inflammatory Proteins ; biosynthesis ; genetics ; Receptors, CCR1 ; Receptors, CCR2 ; Receptors, Chemokine ; biosynthesis ; genetics ; Tumor Cells, Cultured

Alcoholism ; metabolism ; Animals ; Brain ; metabolism ; Chemokine CCL2 ; genetics ; metabolism ; Male ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, CCR2 ; genetics ; metabolism

OBJECTIVE: To explore the microvessel counts and the expressions of interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory protein-1 ( MIP-1) alpha mRNA in the pathological scar tissues. METHODS: Immunohistochemical method of avidin-biotin complex was used for microvessel counts on the routinely formalin-fixed and paraffin-embedded sections of specimens of hypertrophic scars, keloids, normal skin, and surgical scar, and in situ hybridization for the expressions of IL-8, MCP-1, MIP-1alpha mRNA. RESULTS: The microvessel counts as well as the positive rates and the scorings of IL-8, MCP-1, and MIP-1alpha mRNA were significantly higher in pathological scars than those in the normal skin and surgical scar (all P < 0.05). The microvessel counts were significantly higher in the positive cases of IL-8, MCP-1 and MIP-1alpha mRNA than those in the negative ones (P < 0.05). The close positive correlations were found among the microvessel counts and the expressive scorings of 3 factors (P < 0.05). The close positive correlations were also found among the expressive scorings of IL-8, MCP-1, and MIP-1alpha mRNA in pathological scars. Microvessel counts were significantly higher in hypertrophic scars with the course less than 1 year than those with the course more than 1 year. CONCLUSION IL-8, MCP-1 and MIP-1alpha play important roles in promoting the neovascularization of pathological scars.
Adolescent ; Adult ; Burns ; complications ; Capillaries ; metabolism ; Chemokine CCL2 ; biosynthesis ; genetics ; Chemokine CCL3 ; Chemokine CCL4 ; Cicatrix ; etiology ; metabolism ; Female ; Humans ; Interleukin-8 ; biosynthesis ; genetics ; Macrophage Inflammatory Proteins ; biosynthesis ; genetics ; Male ; Middle Aged ; RNA, Messenger ; biosynthesis ; genetics ; Skin ; blood supply

Objective To investigate the effects of miR-877-3p on migration and apoptotic T lymphocytes of bone mesenchymal stem cells (BMSCs). Methods The model of osteoporosis induced by bilateral ovariectomy (OVX) and sham operation was established. At 8 weeks after operation, the bone parameters of the two groups were detected by micro-CT. The levels of monocyte chemotactic protein 1(MCP-1) in BMSCs were detected by ELISA. BMSC in OVX group and sham group were co-cultured with T lymphocytes, respectively. The migration ability of T lymphocytes in the two groups was observed by Transwell^TM assay with PKH26 staining and apoptosis of T lymphocytes were detected by flow cytometry. Reverse transcription PCR was used to detect the expression of miR-877-3p in BMSCs. miR-877-3p was overexpressed or down-regulated by cell transfection. The level of MCP-1 secreted by BMSCs in each group was detected by ELISA. The migration and apoptosis of T lymphocytes were detected by the above methods. Results The number of trabecular bone and bone mineral density in OVX group were lower than those in sham group. The levels of MCP-1 secretion, chemotactic and apoptotic T lymphocyte ability of BMSCs in OVX group were also lower than those in sham group. The expression level of miR-877-3p in BMSC in OVX group was higher than that in sham group. After overexpression of BMSC miR-877-3p, the levels of MCP-1 secreted from BMSCs, and apoptotic T lymphocytes decreased, while the results were opposite after down-regulation of miR-877-3p. Conclusion miR-877-3p may be one of the causes of osteoporosis by inhibiting MCP-1 secretion of BMSCs and the migration and apoptosis of T lymphocytes.
Animals ; Female ; Mice ; Apoptosis/genetics* ; Bone Marrow Cells/metabolism* ; Cell Differentiation ; Chemokine CCL2/metabolism* ; Mesenchymal Stem Cells/metabolism* ; MicroRNAs/metabolism* ; Osteogenesis ; Osteoporosis/genetics* ; T-Lymphocytes/metabolism*

OBJECTIVETo elucidate the roles of monocyte chemotactic factors (MCP-1, RANTES and Fractalkine) on the vulnerability of atherosclerotic plaques in patients with stable (SAP) and unstable angina pectoris (UAP).

METHODSPatients with SAP (n = 50) and UAP (n = 50) underwent coronary angiography (CAG) and intravenous ultrasound (IVUS) were included in the study. Monocyte chemotaxis was assayed by the transwell chamber. Concentrations of hs-CRP, MCP-1, RANTES and Fractalkine were measured by Enzyme-linked-immunosorbent assay (ELISA). mRNA expression of MCP-1, RANTES and Fractalkine in the monocytes was detected by RT-PCR.

RESULTSIVUS evidenced soft lipid plaques in 48% UAP patients and in 16% SAP patients (P < 0.05). SAP patients had mainly fibrous and mixed plaques. Plaque burden and vascular remodeling index were significantly higher in UAP patients than in SAP patients (P < 0.01). The averaged number of migrated monocytes in the UAP patients were higher than that in patients with SAP (P < 0.01). Concentration of hs-CRP, MCP-1, RANTES and Fractalkine were significantly higher in UAP patients than those of SAP patients (P < 0.05 or P < 0.01). mRNA expression of MCP-1, RANTES and Fractalkine in patients with UAP was significantly higher than those of SAP patients (P < 0.05).

CONCLUSIONUpregulated monocyte chemotactic factors (MCP-1, RANTES and Fractalkine) might promote coronary plaque vulnerability in UAP patients.

Angina Pectoris ; metabolism ; pathology ; Angina, Unstable ; metabolism ; pathology ; Chemokine CCL2 ; metabolism ; Chemokine CCL5 ; metabolism ; Chemokine CX3CL1 ; metabolism ; Coronary Angiography ; Female ; Humans ; Male ; Middle Aged ; Plaque, Atherosclerotic ; pathology ; RNA, Messenger ; genetics

OBJECTIVETo investigate the effects of very low-density lipoprotein (VLDL) on cellular lipid accumulation and the expression of monocyte chemoattractant protein-1 (MCP-1) in human mesangial cells.

METHODSAn established stable human mesangial cell line (HMCL) was used in all experiments. VLDL-induced cellular lipid deposition was visualized by Oil Red O staining and analyzed quantitatively by standard enzymatic procedures. MCP-1 mRNA and protein expression levels in treated HMCLs were determined by real-time quantitative RT-PCR and enzyme-linked immunosorbent assay, respectively. For adhesion study, HMCLs were treated with VLDL for 12 hours, followed by a one-hour incubation with THP-1 cells.

RESULTSVLDL induced cellular lipid accumulation in HMCLs in a time- (0-24 h) and dose- (0-200 microg/ml) dependent manner, and the principal component of accumulated lipid is triglyceride. In HMCLs, MCP-1 mRNA expression was promoted by VLDL in a time- (0-6 h) and dose- (0-100 microg/ml) dependent manner, and VLDL also enhanced MCP-1 secretion in a dose-dependent manner. Such an effect was accompanied by increased adhesion of monocytes to HMCLs.

CONCLUSIONSVLDL can induce cellular triglyceride accumulation and upregulate the expression of MCP-1 in human mesangial cells. Hence, VLDL may be involved in the pathogenesis of lipid-mediated renal injury.

Cell Line ; Chemokine CCL2 ; genetics ; metabolism ; Humans ; Lipoproteins, VLDL ; pharmacology ; toxicity ; Mesangial Cells ; cytology ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Triglycerides ; metabolism

OBJECTIVETo determine the role of the novel proinflammatory cytokine high mobility group box chromosomal protein 1 (HMGB-1) in the pathogenesis of lupus nephritis.

METHODSSerum levels of anti-dsDNA antibodies were determined by enzyme linked immunosorbent assay (ELISA). Renal morphologic features were examined by light microscopy, electron microscopy, and immunohistologic analyses. The mRNA expression of HMGB-1 and monocyte chemoattractant protein-1 (MCP-1) was detected by RT-PCR.

RESULTMRL/lpr mice demonstrated characteristic alterations of serum immune parameters, with progressively increased anti-dsDNA antibodies with age, compared with age-matched C57BL/6J mice. MRL/lpr mice showed progressive development of renal damage, starting at 12 weeks of age and reached the peak at 20 weeks. The observed lesions included the presence of enlarged hypercellular glomeruli, with increased numbers of both resident cells and infiltrating leukocytes. Higher expression of HMGB-1 mRNA was found in MRL/lpr mice than what in C57BL/6J mice. Expression of HMGB-1 was positively correlated with that of MCP-1 mRNA.

CONCLUSIONThe results demonstrate that the higher expression of HMGB-1 may contribute to the pathogenesis of lupus nephritis.

Animals ; Chemokine CCL2 ; metabolism ; Disease Models, Animal ; HMGB1 Protein ; genetics ; metabolism ; Kidney ; metabolism ; pathology ; Lupus Nephritis ; metabolism ; pathology ; Mice ; Mice, Inbred MRL lpr ; RNA, Messenger ; genetics

OBJECTIVEKawasaki disease (KD) is a febrile illness of childhood. The etiology of KD remains unknown. Multiple theories exist, including an infectious etiology and an immunological abnormality. Cardiac involvement ranges from myocarditis and pericarditis in the acute stage to the development of coronary artery aneurysms later in the course. The present study aimed to explore the effect of monocyte chemotactic protein-1 (MCP-1) in Kawasaki disease and its relationship with damage to the coronary arteries during the development of KD.

METHODSPlasma MCP-1 concentrations were measured by enzyme-linked immunosorbent assay (ELISA), and MCP-1 mRNA expression in peripheral blood mononuclear cells (PBMC) was measured by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) in comparison of three groups: 56 patients with KD, 60 age-matched patients with non-infectious diseases, and 66 age-matched febrile patients with various diseases.

RESULTSPlasma MCP-1 concentration and MCP-1 mRNA expression in PBMC of patients with active KD [(409.55 +/- 97.42) pg/ml] and (1.97 +/- 0.77) were higher than those of control group. Plasma MCP-1 levels and MCP-1 mRNA expression of inactive KD group [(301.64 +/- 71.55) pg/ml] and (1.31 +/- 0.39) were significantly higher than those of non-infectious diseases patients. There was a marked increase in patients with inactive KD than those of non-infective patients, but there were no significant differences between inactive KD and febrile patients. Plasma MCP-1 levels and MCP-1 mRNA expression were markedly increased in KD patients with coronary artery lesions than those in patients without coronary artery lesions.

CONCLUSIONPlasma MCP-1 concentration and MCP-1 mRNA expression in PBMC were significantly increased in patients with KD, and they were higher in KD with coronary artery lesions. It indicates that MCP-1 may be a useful parameter for monitoring disease activity in patients with KD.

Chemokine CCL2 ; blood ; genetics ; metabolism ; Child ; Child, Preschool ; Coronary Vessels ; pathology ; Female ; Humans ; Infant ; Leukocytes, Mononuclear ; metabolism ; Male ; Mucocutaneous Lymph Node Syndrome ; blood ; genetics ; pathology ; RNA, Messenger ; genetics

OBJECTIVETo explore the role of monocyte chemoattractant protein-1 (MCP-1) in lupus nephritis (LN).

METHODSSera MCP-1 levels were measured by enzyme linked immunosorbent assay in 112 patients with systemic lupus erythematosus (SLE), 30 patients with rheumatoid arthritis, 11 non-SLE patients with renal impairment, and 40 healthy volunteers. MCP-1 mRNA expression in peripheral blood mononuclear cells (PBMCs) was also investigated with reverse trancription-polymerase chain reaction semi-quantitative method.

RESULTSThe expression of MCP-1 was significantly higher in active LN groups than in all other groups (P < 0.001), and there was a close correlation between MCP-1 expression and the overall SLE disease activity index score (r=0.6245, P < 0.001) and the SLE disease activity index renal score (r=0.6808, P < 0.001). Low expression of MCP-1 was observed in diseased controls and healthy controls. The sera levels of MCP-1 were significantly higher in patients with active diseases than in patients with inactive SLE and controls, but no significant difference were found between the active LN groups and non-renal involvement group (P >0.05).

CONCLUSIONThe expression of PBMCs MCP-1 mRNA is upregulated in active SLE. Meanwhile, its expression levels are correlated with the activity of LN.

Adolescent ; Adult ; Aged ; Arthritis, Rheumatoid ; metabolism ; Chemokine CCL2 ; biosynthesis ; genetics ; Female ; Humans ; Lupus Erythematosus, Systemic ; metabolism ; Lupus Nephritis ; metabolism ; Male ; Middle Aged ; RNA, Messenger ; biosynthesis ; genetics