Abstract:
OBJECTIVE:Individuals with inflammation have a myriad of pregnancy aberrations including increasing their preterm birth risk. Toll-like receptors (TLRs) and receptor for advanced glycation end products (RAGE) and their ligands were all found to play a key role in inflammation. In the present study, we reviewed TLR and RAGE expression, their ligands, and signaling in preterm birth. RESEARCH DESIGN AND METHODS:A systematic search was performed in the electronic databases PubMed and ScienceDirect up to July 2010, combining the keywords "preterm birth," "TLR", "RAGE", "danger signal", "alarmin", "genomewide," "microarray," and "proteomics" with specific expression profiles of genes and proteins. RESULTS:This paper provides data on TLR and RAGE levels and critical downstream signaling events including NF-kappaB-dependent proinflammatory cytokine expression in preterm birth. About half of the genes and proteins specifically present in preterm birth have the properties of endogenous ligands "alarmin" for receptor activation. The interactions between the TLR-mediated acute inflammation and RAGE-mediated chronic inflammation have clear implications for preterm birth via the TLR and RAGE system, which may be acting collectively. CONCLUSIONS:TLR and RAGE expression and their ligands, signaling, and functional activation are increased in preterm birth and may contribute to the proinflammatory state.
journal_name
Mediators Inflammjournal_title
Mediators of inflammationauthors
Noguchi T,Sado T,Naruse K,Shigetomi H,Onogi A,Haruta S,Kawaguchi R,Nagai A,Tanase Y,Yoshida S,Kitanaka T,Oi H,Kobayashi Hdoi
10.1155/2010/490406subject
Has Abstractpub_date
2010-01-01 00:00:00pages
490406eissn
0962-9351issn
1466-1861journal_volume
2010pub_type
杂志文章,评审abstract::Postoperative cognitive dysfunction (POCD) increases morbidity and mortality after surgery. But the underlying mechanism is not clear yet. While age is now accepted as the top one risk factor for POCD, results from studies investigating postoperative cognitive functions in adults have been controversial, and data abou...
journal_title:Mediators of inflammation
pub_type: 杂志文章
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abstract::With the development of culture-independent techniques, numerous studies have demonstrated that the lower airway is not sterile in health and harbors diverse microbial communities. Furthermore, new evidence suggests that there is a distinct lower airway microbiome in those with chronic respiratory disease. To understa...
journal_title:Mediators of inflammation
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abstract::Endothelial dysfunction is regarded as an important factor in the pathogenesis of vascular disease in obesity-related type 2 diabetes. The imbalance in repair and injury (hyperglycemia, hypertension, dyslipidemia) results in microvascular changes, including apoptosis of microvascular cells, ultimately leading to diabe...
journal_title:Mediators of inflammation
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abstract::Resistin has been shown to cause insulin resistance and to impair glucose tolerance in rodents, but in humans its physiological role still remains elusive. The aim of this study was to examine whether resistin mRNA expression in human peripheral mononuclear cells (PBMCs) and its corresponding plasma levels are altered...
journal_title:Mediators of inflammation
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abstract:Background:Sepsis-induced myocardial dysfunction is a severe clinical problem. Recent studies have indicated that autophagy and myocardial energy depletion play a major role in myocardial dysfunction during sepsis, a mechanistic target of rapamycin (mTOR) as a master sensor of energy status and autophagy mediator; howe...
journal_title:Mediators of inflammation
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abstract::Human periodontal ligament (hPDL) fibroblasts play a major role during periodontitis and orthodontic tooth movement, mediating periodontal inflammation, osteoclastogenesis, and collagen synthesis. The highly COX-2-selective NSAID etoricoxib has a favorable systemic side effect profile and high analgesic efficacy, part...
journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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abstract::The effects of chronic mild prenatal stress on leukocyte infiltration into the airways was investigated in rat offspring. The chronic prenatal stress consisted of transitory and variable changes in the rat's living conditions. Offspring at adult age were actively sensitized (day 0) and intratracheally challenged (day ...
journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
pub_type: 杂志文章,随机对照试验
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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abstract::In addition to its well-established effect on T cells, cyclosporin A (CsA) also inhibits inflammatory cytokine production by macrophages. However, little is known about the mechanism of action of CsA on macrophage cytokine production. We measured the effect of CsA on basal and phorbol-myristate-acetate (PMA)-stimulate...
journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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pub_type: 临床试验,杂志文章
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
pub_type: 杂志文章,评审
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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更新日期:1995-01-01 00:00:00