• 대한의생명과학회지
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• 제14권3호
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• pp.199-201
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• 2008

Eosinophil is an improtant leukocyte in the development of various inflammatory diseases. Monocyte chemoattractant protein-1 (MCP-1) acts as a key regulator on monocyte movement, and activation of T cells and NK cells. However, the role of MCP-1 in eosinophils remains to be solved. In the present study, we examined the effect of MCP-1 on eosinophil migration, using human eosinophilic EoL-1 cells as an in vitro model of eosinophils. The surface expression of CCR2 in EoL-1 cells was little detected but MCP-1 strongly induced EoL-1 cell migration in a dose-dependent manner. Increased chemotactic activity due to MCP-1 was blocked by pertussis toxin, a $G_i/G_o$ protein inhibitor and U73122, a phospholipase C (PLC) inhibitor. These results suggest that MCP-1 activates $G_i/G_o$ protein and PLC and this signal pathway is involved in eosinphil movement. This finding supports the elucidation of pathogenic mechanism of eosinophilic inflammation such as asthma and atopic dermatitis.

• Restorative Dentistry and Endodontics
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• 제25권2호
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• pp.212-218
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• 2000

The recruitment of leukocytes to a site of inflammation is dependent on a complex interplay of a number of cytokines. Monocyte chemoattractant protein-1 (MCP-1) is a potent chemoattractant for monocytes, whereas interleukin-8 (IL-8) has chemotactic activity for neutrophils, lymphocytes, and basophils. The purpose of this study was to determine the effects of several microbes found in infected root canal systems on the production of inflammatoy cytokines, interleukin 8 and monocyte chemoattractant protein-1 from human peripheral blood mononuclear cells (PBMC). Monocytes isolated from peripheral blood were stimulated by group A streptococci (GAS, ATCC 19615), Enterococcus faecalis (ATCC 29212), Streptococcus mutans (ATCC 10449), Streptococcus sanguis (clinical isolate), and Candida albicans (ATCC 90029) respectively. Each of these bacteria induced dose-dependent induction in IL-8 and MCP-1 determined by ELISA. IL-8 production by each bacteria was decreased in the range of the microbe-to-PBMC ratios of 0.1-1.0. Group A streptococci was the week inducer of MCP-1 production. These results suggest that different oral pathogens induce specific dose-dependent patterns of cytokine release. Such patterns may provide a means of control of the type of immune celles particularly with regard to inflammatory leukocyte recruitment.

• 대한의생명과학회지
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• 제17권3호
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• pp.261-265
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• 2011

Parkin is a putative tumor suppressor protein and its expression is frequently reduced or absent in several types of tumors. In this study, we examined the role of Parkin in mRNA expression of monocyte chemotactic protein-1 (MCP-1) in the breast cancer cell line MCF7. Expression of MCP-1 mRNA increased after TNF-${\alpha}$ treatment. However, overexpression of Parkin induced a decrease in expression of MCP-1 mRNA in TNF-${\alpha}$-stimulated MCF7. This decrease in MCP-1 mRNA by Parkin overexpression occurred in a dose- and time-dependent manner. Using a wound scratch assay, we found that Parkin overexpression in MCF7 cells also resulted in a decrease in cell migration. These results suggest that Parkin down-regulates MCP-1 synthesis leading to decreased migration of tumor cells. We suggest that one possible mechanism by which Parkin acts as a tumor suppressor is by inhibiting migration or metastasis of cancer cells.

• The Korean Journal of Physiology and Pharmacology
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• 제15권2호
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• pp.115-122
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• 2011

The aim of this study was to investigate whether matrix metalloproteinase (MMP) inhibitors attenuate neuroinflammation in an ischemic brain following photothrombotic cortical ischemia in mice. Male C57BL/6 mice were anesthetized, and Rose Bengal was systemically administered. Permanent focal ischemia was induced in the medial frontal and somatosensory cortices by irradiating the skull with cold white light. MMP inhibitors, such as doxycycline, minocycline, and batimastat, significantly reduced the cerebral infarct size, and the expressions of monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), and indoleamine 2,3-dioxygenase (IDO). However, they had no effect on the expressions of heme oxygenase-1 and neuroglobin in the ischemic cortex. These results suggest that MMP inhibitors attenuate ischemic brain injury by decreasing the expression levels of MCP-1, TNF-${\alpha}$, and IDO, thereby providing a therapeutic benefit against cerebral ischemia.

• 방사선산업학회지
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• 제4권3호
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• pp.227-231
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• 2010

The purpose of this study was to investigate the expression mechanism of MCP-1 in gamma-irradiated RAW 264.7 macrophage cells. MCP-1 plays an important role in attracting monocyte to injured site at the early inflammation stage. However the production mechanism of MCP-1 by gamma-irradiation in RAW 264.7 macrophage cells was almost undiscovered. We found that MCP-1 was produced in RAW 264.7 macrophage cells by irradiation with 5 Gy. And these inceases were attenuated by specific inhibitors treatment, such as $NF-{\kappa}B$, JNK, ERK, JAK2, and Pyk2. These results indicate that radiation-induced MCP-1 production is mediated by MyD88- and TRIF-dependent pathways in RAW 264.7 macrophage cells. Furthermore, gamma-irradiation induced heme oxygenase-1 (HO-1) expression in RAW 264.7 macrophage cells. However this induction level was reduced before MCP-1 and $IFN-{\beta}$ production.

• Korean Circulation Journal
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• 제48권11호
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• pp.1014-1024
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• 2018

Background and Objectives: Intense exercise (IE) induced myocardial fibrosis (MF) showed contradictory findings in human studies, making the relationship between IE and the development of MF unclear. This study aims to demonstrate exercise induced MF is associated with cardiac damage, and inflammation is essential to the development of exercise induced MF. Methods: Sprague-Dawley rats were submitted to daily 60-minutes treadmill exercise sessions at vigorous or moderate intensity, with 8-, 12-, and 16-week durations; time-matched sedentary rats served as controls. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum cardiac troponin I (cTnI) concentration. After completion of the exercise protocol rats were euthanized. Biventricular morphology, ultrastructure, and collagen deposition were then examined. Protein expression of interleukin $(IL)-1{\beta}$ and monocyte chemotactic protein (MCP)-1 was evaluated in both ventricles. Results: After IE, right but not left ventricle (LV) MF occurred. Serum cTnI levels increased and right ventricular damage was observed at the ultrastructure level in rats that were subjected to long-term IE. Leukocyte infiltration into the right ventricle (RV) rather than LV was observed after long-term IE. Long-term IE also increased protein expression of proinflammation factors including $IL-1{\beta}$ and MCP-1 in the RV. Conclusions: Right ventricular damage induced by long-term IE is pathological and the following inflammatory response is essential to the development of exercise induced MF.

• BMB Reports
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• 제38권1호
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• pp.77-81
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• 2005

The monocyte chemotactic protein-3 (MCP3), on chromosome 17q11.2-q12, is a secreted chemokine, which attracts macrophages during inflammation and metastasis. In an effort to discover additional polymorphism(s) in genes whose variant(s) have been implicated in asthma, we scrutinized the genetic polymorphisms in MCP3 to evaluate it as a potential candidate gene for asthma host genetic study. By direct DNA sequencing in twenty-four individuals, we identified four sequence variants within the 3 kb full genome including 1,000bp promoter region of MCP3; one in promoter region (-420T>C), three in intron (+136C>G, +563C>T, +984G>A) respectively. The frequencies of those four SNPs were 0.020 (-420T>C), 0.038 (+136C>G), 0.080 (+563C>T), 0.035 (+984G>A), respectively, in Korean population (n = 598). Haplotypes, their frequencies and linkage disequilibrium coefficients (|D'|) between SNP pairs were estimated. The associations with the risk of asthma, skin-test reactivity and total serum IgE levels were analyzed. Using statistical analyses for association of MCP3 polymorphisms with asthma development and asthma-related phenotypes, no significant signals were detected. In conclusion, we identified four genetic polymorphisms in the important MCP3 gene, but no significant associations of MCP3 variants with asthma phenotypes were detected. MCP3 variation/haplotype information identified in this study will provide valuable information for future association studies of other allergic diseases.

• 한방재활의학과학회지
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• 제33권3호
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• pp.33-46
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• 2023

Objectives We investigated anti-obesity effects of Menthae Herba hydrosol in obese mice. Methods Animals were divided into four groups, and treatments were performed for 7 weeks. After the treatment, serum lipid profiles, weight and pathological morphology in liver, kidney, adipose tissue were measured. Also, hepatic protein and gene expression levels of lipid metabolism-related factors were analyzed. Results Body weight was decreased in P3% group. In P1% (group fed high-fat diet and 1% Menthae Herba hydrosol) and P3% (group fed high-fat diet and 3% Menthae Herba hydrosol) group, weight of white adipose tissue, serum levels of triglyceride and blood urea nitrogen were decreased, and weight of muscle was increased. Also, liver, kidney and epididymal adipocyte size were reduced in P1% and P3% group. Adenosine monophosphate-activated protein kinase was increased and sterol regulatory element binding protein-1c (SREBP-1c) was decreased in P3% group. mPeroxisome proliferator-activator receptor-γ, mMonocyte chemotactic protein-1 were decreased in P1% and P3% group. In P3% group, mSREBP-1c was decreased and mCarnitine palmitoyl transferase-1 was increased. And mUncoupling protein 1 in brown adipose tissue was increased. Conclusions These results suggest that Menthae Herba hydrosol has a worthy effect on anti-obesity.

• Animal cells and systems
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• 제13권4호
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• pp.391-397
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• 2009

The house dust mite (Dermatophagoides pteronissinus) is an important factor in triggering allergic diseases. The function of eosinophils, particularly in the production of cytokine or chemokine, is critical in understanding the pathogenesis of inflammatory diseases. In this study, we examined whether D. pteronissinus extract (DpE) induces the expression of monocyte chemotactic protein 1 (MCP-1)/CCL2, IL-8/CXCL8, and IL-6 that mediate in the infiltration and activation of immune cells and in its signaling mechanism in the human eosinophilic cell line, EoL-1. DpE increased the mRNA and protein expression of MCP-1, IL-8, and IL-6 in a time- and dose-dependent course in EoL-1 cells. In our experiments using signal-specific inhibitors, we found that the increased expression of MCP-1, IL-8, and IL-6 due to DpE is associated with Src family tyrosine kinase and protein kinase C $\delta$ (PKC $\delta$). In addition, the activation of extracellular signal-regulated kinase (ERK) is required for MCP-1 and IL-8 expression while p38 mitogen-activated protein kinase (MAPK) is involved in IL-6 expression. DpE induced the phosphorylation of ERK and p38 MAPK. PP2, an inhibitor of Src family tyrosine kinase, and rottlerin, an inhibitor of PKC $\delta$, blocked the activation of ERK and p38 MAPK. DpE induces the activation of ERK and p38 MAPK via Src family tyrosine kinase and PKC $\delta$ for MCP-1, IL-8, or IL-6 production. Increased cytokine release due to the house dust mite and the characterization of its signal transduction may be valuable in understanding the eosinophil-related pathogenic mechanism of inflammatory diseases.

• 대한본초학회지
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• 제29권1호
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• pp.1-6
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• 2014

Objectives : Many of currently used anti-cancer drugs were developed to target cell death mechanisms and had serious side effects by causing damage to normal cells. Hangambujeongsan or Kangai Fuzheng Powder was a mixture based on the traditional Chinese medicine. It had been used in the local Chinese hospitals to treat cancer patients for decades and had shown a certain level of beneficial effects without major toxic effects. But its mechanism of action had not been elucidated yet. Thus this study aimed to investigate the effects of Kangai Fuzheng Powder in an in vitro experiment. Methods : Cancer lines or RAW264.7 mouse macrophage cells were treated with Kangai Fuzheng Powder. Cell viability was measured by MTT assay, and morphological observation was also performed. Gene expression of cytokines in macrophages was determined by real-time polymerase chain reaction. Phagocytic function assay was also performed in macrophage cells. Results : Kangai Fuzheng Powder had no direct detrimental effect on cancer cells. When macrophages were co-cultured with cancer cells, Kangai Fuzheng Powder had toxic effect on cancer cells. After exposing macrophages to Kangai Fuzheng Powder, macrophages transformed into activated form and the mRNA level of tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, interleukin-10 and monocyte chemotactic protein-1 was significantly enhanced. Phagocytic activity of macrophages was dramatically potentiated. Conclusions : We demonstrated that anti-cancer effect of Kangai Fuzheng Powder was related to activation of macrophages including enhanced cytokine production and phagocytic function.