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Monocyte chemoattractant protein (MCP)-1 -2518 A/G SNP in Chinese Han patients with VKH syndrome.

ABSTRACT: PURPOSE: Vogt-Koyanagi-Harada (VKH) syndrome is an autoimmune disease. The monocyte chemoattractant protein-1 (MCP-1) gene has been implicated in the pathogenesis of certain autoimmune diseases. The aim of this study was to examine whether a MCP-1 polymorphism was associated with VKH syndrome. METHODS: A case-control analysis was performed using genomic DNA samples from 307 VKH patients and 319 age-, sex-, and ethnically-matched healthy controls. The MCP-1 polymorphism at the -2518 A/G locus was genotyped using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) assay. RESULTS: The distribution of genotypic frequency of the MCP-1 -2518 A/G polymorphism in all subjects did not deviate from Hardy-Weinberg equilibrium (HWE; p>0.05). Allelic and genotypic frequency analysis revealed no significant difference between VKH patients and healthy controls for the MCP-1 -2518 A/G polymorphism (p>0.05). No significant differences were found according to gender and neither was found according to extraocular findings including neck stiffness, tinnitus, alopecia, poliosis, dysacusia, scalp hypersensitivity, and vitiligo. CONCLUSIONS: The result suggests that the susceptibility to VKH syndrome in Chinese Han patients may be not influenced by the MCP-1 -2518 A/G polymorphism.

SUBMITTER: Hou S

PROVIDER: S-EPMC2722713 | biostudies-literature | 2009

REPOSITORIES: biostudies-literature

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Monocyte chemoattractant protein (MCP)-1 -2518 A/G SNP in Chinese Han patients with VKH syndrome.

Hou Shengping S Yang Peizeng P Xie Lin L Du Liping L Zhou Hongyan H Jiang Zhengxuan Z

Molecular vision 20090808

<h4>Purpose</h4>Vogt-Koyanagi-Harada (VKH) syndrome is an autoimmune disease. The monocyte chemoattractant protein-1 (MCP-1) gene has been implicated in the pathogenesis of certain autoimmune diseases. The aim of this study was to examine whether a MCP-1 polymorphism was associated with VKH syndrome.<h4>Methods</h4>A case-control analysis was performed using genomic DNA samples from 307 VKH patients and 319 age-, sex-, and ethnically-matched healthy controls. The MCP-1 polymorphism at the -2518 ...[more]

PMID: 19668598

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Project description:BackgroundCancer-associated wasting, termed cancer cachexia, has a profound effect on the morbidity and mortality of cancer patients but remains difficult to recognize and diagnose. While increases in circulating levels of a number of inflammatory cytokines have been associated with cancer cachexia, these associations were generally made in patients with advanced disease and thus may be associated with disease progression rather than directly with the cachexia syndrome. Thus, we sought to assess potential biomarkers of cancer-induced cachexia in patients with earlier stages of disease.MethodsA custom multiplex array was used to measure circulating levels of 25 soluble factors from 70 pancreatic cancer patients undergoing attempted tumour resections. A high-sensitivity multiplex was used for increased sensitivity for nine cytokines.ResultsResectable pancreatic cancer patients with cachexia had low levels of canonical pro-inflammatory cytokines including interleukin-6 (IL-6), interleukin-1β (IL-1β), interferon-γ (IFN-γ), and tumour necrosis factor (TNF). Even in our more sensitive analysis, these cytokines were not associated with cancer cachexia. Of the 25 circulating factors tested, only monocyte chemoattractant protein-1 (MCP-1) was increased in treatment-naïve cachectic patients compared with weight stable patients and identified as a potential biomarker for cancer cachexia. Although circulating levels of leptin and granulocyte-macrophage colony-stimulating factor (GM-CSF) were found to be decreased in the same cohort of treatment-naïve cachectic patients, these factors were closely associated with body mass index, limiting their utility as cancer cachexia biomarkers.ConclusionsUnlike in advanced disease, it is possible that cachexia in patients with resectable pancreatic cancer is not associated with high levels of classical markers of systemic inflammation. However, cachectic, treatment-naïve patients have higher levels of MCP-1, suggesting that MCP-1 may be useful as a biomarker of cancer cachexia.

Project description:Parathyroid hormone (PTH) is necessary for the regulation of calcium homeostasis and PTH (1-34) was the first approved osteoanabolic therapy for osteoporosis. It is well established that intermittent PTH increases bone formation and that bone remodeling and several cytokines and chemokines play an essential role in this process. Earlier, we had established that the chemokine, monocyte chemoattractant protein-1 (MCP-1/CCL2), was the most highly stimulated gene in rat bone after intermittent PTH injections. Nevertheless, MCP-1 function in bone appears to be complicated. To identify the primary cells expressing MCP-1 in response to PTH, we performed in situ hybridization of rat bone sections after hPTH (1-34) injections and showed that bone-lining osteoblasts are the primary cells that express MCP-1 after PTH treatment. We previously demonstrated MCP-1's importance by showing that PTH's anabolic effects are abolished in MCP-1 null mice, further implicating a role for the chemokine in this process. To establish whether rhMCP-1 peptide treatment could rescue the anabolic effect of PTH in MCP-1 null mice, we treated 4-month-old wild-type (WT) mice with hPTH (1-34) and MCP-1-/- mice with rhMCP-1 and/or hPTH (1-34) for 6 weeks. Micro-computed tomography (μCT) analysis of trabecular and cortical bone showed that MCP-1 injections for 6 weeks rescued the PTH anabolic effect in MCP-1-/- mice. In fact, the combination of rhMCP-1 and hPTH (1-34) has a synergistic anabolic effect compared with monotherapies. Mechanistically, PTH-enhanced transforming growth factor-β (TGF-β) signaling is abolished in the absence of MCP-1, while MCP-1 peptide treatment restores TGF-β signaling in the bone marrow. Here, we have shown that PTH regulates the transcription of the chemokine MCP-1 in osteoblasts and determined how MCP-1 affects bone cell function in PTH's anabolic actions. Taken together, our current work indicates that intermittent PTH stimulates osteoblastic secretion of MCP-1, which leads to increased TGF-β signaling, implicating it in PTH's anabolic actions.

Dataset Information

Monocyte chemoattractant protein (MCP)-1 -2518 A/G SNP in Chinese Han patients with VKH syndrome.

Publications

Monocyte chemoattractant protein (MCP)-1 -2518 A/G SNP in Chinese Han patients with VKH syndrome.

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