72 research outputs found

    Comparison of Protein Profiles of Gingival Crevicular Fluids Collected from Incisors, Canines, and Molars

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    Many studies have shown that gingival crevicular fluid (GCF) reflects the inflammatory state of local periodontal tissues. GCF has been collected from several types of teeth in previous studies. However, there is no report that characterizes GCF by the type of tooth. In the present study, the protein profiles of GCF from different sites were comprehensively compared with each other. GCF was sampled from six healthy adult men (21-31 years old) with healthy periodontal tissues. Three separate GCF samples were collected at the maxillary central incisor, canine, and first molar of each individual. The protein profiles of GCF were analyzed using sodium dodecyl sulfate polyacrylamide gel electrophoresis and liquid chromatogram-tandem mass spectrometry (LC-MS/MS). The band patterns on the sodium dodecyl sulfate polyacrylamide gel electrophoresis from the set of three GCF samples from each individual were similar, regardless of the type of tooth. The proteins contained in each band were identified by LC-MS/MS analysis, and they were found to be the same among the three GCF samples. A comprehensive and quantitative analysis of proteins in the GCF samples was performed by LC-MS/MS using isobaric tag labeling. In total, 86 proteins were identified in GCF. A small number of proteins were increased or decreased in GCF from the first molars compared with the other types of teeth in one or two individuals. However, overall, no proteins were found to exhibit a reproducibly different composition in any of the individuals. These analyses show that the protein profiles of GCF in healthy periodontal tissues are similar, regardless of the type of tooth

    Expression of nephronectin is inhibited by oncostatin M via both JAK/STAT and MAPK pathways

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    AbstractNephronectin (Npnt), also called POEM, is an extracellular matrix protein considered to play critical roles as an adhesion molecule in the development and functions of various tissues, such as the kidneys, liver, and bones. In the present study, we examined the molecular mechanism of Npnt gene expression and found that oncostatin M (OSM) strongly inhibited Npnt mRNA expression in MC3T3-E1 cells from a mouse osteoblastic cell line. OSM also induced a decrease in Npnt expression in both time- and dose-dependent manners via both the JAK/STAT and MAPK pathways. In addition, OSM-induced inhibition of osteoblast differentiation was recovered by over-expression of Npnt. These results suggest that OSM inhibits Npnt expression via the JAK/STAT and MAPK pathways, while down-regulation of Npnt by OSM influences inhibition of osteoblast differentiation

    Integral role of receptor for advanced glycation end products (RAGE) in nondiabetic atherosclerosis

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    An advanced glycation end products (AGE)/a receptor for AGE (RAGE) axis plays a central role in the pathogenesis of diabetic vascular remodeling. This study was conducted to clarify the role of RAGE in nondiabetic atherosclerosis. We used the aortic and coronary atherosclerotic lesions of Watanabe heritable hyperlipidemic (WHHL) rabbits prone to myocardial infarction (WHHLMI) at 1 to 14 months. Immunohistochemistry demonstrated the significant expression of RAGE as early as at 1 month with the stronger expression at 3 and 7 months, which was remarkably diminished at 14 months. RAGE expression was concordant with AGE accumulation. The major original sources of RAGE expression were macrophages and smooth muscle cells in addition to endothelial cells, and RAGE expression was distributed in the areas of phospholipid products, a component of oxidized LDL and nitrotyrosine. The concentrations of serum AGE did not alter significantly with aging. These findings suggested the expression of RAGE was induced by hyperlipidemia and oxidative stress independent of diabetes in WHHLMI rabbits. Additionally, our in vitro study showed that silencing of RAGE tended to attenuate oxidized-LDL-triggered PAI-1 expression in human cultured macrophages, as well as oxidized-LDL-induced tissue factor expression in peritoneal macrophages, suggesting a possible role of RAGE in prothrombogenic molecular regulation. In conclusion, the present study provides in vivo evidence that RAGE plays an integral role in the initiation and progression of nondiabetic atherosclerosis, suggesting that RAGE may be a novel target for treating not only diabetic but also nondiabetic vascular complications

    Chronic Exposure to Low Frequency Noise at Moderate Levels Causes Impaired Balance in Mice

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    We are routinely exposed to low frequency noise (LFN; below 0.5 kHz) at moderate levels of 60–70 dB sound pressure level (SPL) generated from various sources in occupational and daily environments. LFN has been reported to affect balance in humans. However, there is limited information about the influence of chronic exposure to LFN at moderate levels for balance. In this study, we investigated whether chronic exposure to LFN at a moderate level of 70 dB SPL affects the vestibule, which is one of the organs responsible for balance in mice. Wild-type ICR mice were exposed for 1 month to LFN (0.1 kHz) and high frequency noise (HFN; 16 kHz) at 70 dB SPL at a distance of approximately 10–20 cm. Behavior analyses including rotarod, beam-crossing and footprint analyses showed impairments of balance in LFN-exposed mice but not in non-exposed mice or HFN-exposed mice. Immunohistochemical analysis showed a decreased number of vestibular hair cells and increased levels of oxidative stress in LFN-exposed mice compared to those in non-exposed mice. Our results suggest that chronic exposure to LFN at moderate levels causes impaired balance involving morphological impairments of the vestibule with enhanced levels of oxidative stress. Thus, the results of this study indicate the importance of considering the risk of chronic exposure to LFN at a moderate level for imbalance

    Searching for Oxidized Low-Density Lipoproteins <i>In Vivo</i>

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    The Dynamics of Oxidized LDL during Atherogenesis

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    Accumulating evidence indicates that oxidized low-density lipoprotein (OxLDL) is a useful marker for cardiovascular disease. The uptake of OxLDL by scavenger receptors leads to the accumulation of cholesterol within the foam cells of atherosclerotic lesions. OxLDL has many stimulatory effects on vascular cells, and the presence of OxLDL in circulating blood has been established. According to the classical hypothesis, OxLDL accumulates in the atherosclerotic lesions over a long duration, leading to advanced lesions. However, recent studies on time-course changes of OxLDL in vivo raised a possibility that OxLDL can be transferred between the lesions and the circulation. In this paper, the in vivo dynamics of OxLDL are discussed

    Perilipins: a diversity of intracellular lipid droplet proteins

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    Abstract Intracellular lipid droplets (LDs) are found in a wide variety of cell types and have been recognized as organelles with unique spherical structures. Although LDs are not stable lipid-depots, they are active sites of neutral lipid metabolism, and comprise neutral lipid or cholesterol cores surrounded by phospholipid monolayers containing specialized proteins. However, sizes and protein compositions vary between cell and tissue types. Proteins of the perilipin family have been associated with surfaces of LDs and all carry a conserved 11-mer repeat motif. Accumulating evidence indicates that all perilipins are involved in LD formation and that all play roles in LD function under differing conditions. In this brief review, we summarize current knowledge of the roles of perilipins and lipid metabolizing enzymes in a variety of mammalian cell types
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