10 research outputs found

    Melanocortins induce interleukin 6 gene expression and secretion through melanocortin receptors 2 and 5 in 3T3-L1 adipocytes

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    Interleukin 6 (IL6) is a pleiotropic cytokine that not only affects the immune system, but also plays an active role in many physiological events in various organs. Notably, 35% of systemic IL6 originates from adipose tissues under noninflammatory conditions. Here, we describe a previously unknown function of melanocortins in regulating Il6 gene expression and production in 3T3-L1 adipocytes through membrane receptors which are called melanocortin receptors (MCRs). Of the five MCRs that have been cloned, MC2R and MC5R are expressed during adipocyte differentiation. α-Melanocyte-stimulating hormone (α-MSH) or ACTH treatment of 3T3-L1 adipocytes induces Il6 gene expression and production in a time- and concentration-dependent manner via various signaling pathways including the protein kinase A, p38 mitogen-activated protein kinase, cJun N-terminal kinase, and IκB kinase pathways. Specific inhibition of MC2R and MC5R expression with short interfering Mc2r and Mc5r RNAs significantly attenuated the α-MSH-induced increase of intracellular cAMP and both the level of Il6 mRNA and secretion of IL6 in 3T3-L1 adipocytes. Finally, when injected into mouse tail vein, α-MSH dramatically increased the Il6 transcript levels in epididymal fat pads. These results suggest that α-MSH in addition to ACTH may function as a regulator of inflammation by regulating cytokine production

    Thermal and Mechanical Degradation of Recycled Polylactic Acid Filaments for Three-Dimensional Printing Applications

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    The recycling of filaments used in three-dimensional (3D) printing systems not only mitigates the environmental issues associated with conventional 3D printing approaches but also simultaneously reduces manufacturing costs. This study investigates the effects of successive recycling of polylactic acid (PLA) filaments, which were used in the printing process, on the mechanical properties of recycled filaments and printed objects. The mechanical strengths of the printed PLA and the adhesion strengths between 3D-printed beads were evaluated via the tensile testing of the horizontally and vertically fabricated specimens. Gel permeation chromatography analysis revealed a reduction in the molecular weight of the polymer as a result of recycling, leading to a decrease in the mechanical strength of the 3D-printed product. Additionally, scanning electron microscopy images of the cutting plane showed that the fabricated beads were broken in the case of the horizontally fabricated specimen, whereas in the case of the vertically fabricated samples, the adhesion between the beads was weak. These findings indicate that the mechanical strength in the in-plane and out-of-plane directions must be improved by increasing the mechanical strength of the bead itself as well as the adhesion strength of the beads

    Proteomic Analysis of Tumor Necrosis Factor-Alpha (TNF-alpha)-Induced L6 Myotube Secretome Reveals Novel TNF-alpha-Dependent Myokines in Diabetic Skeletal Muscle

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    There is a strong possibility that skeletal muscle can respond to irregular metabolic states by secreting specific cytokines. Obesity-related chronic inflammation, mediated by pro-inflammatory cytokines, is believed to be one of the causes of insulin resistance that results in type 2 diabetes. Here, we attempted to identify and characterize the members of the skeletal muscle secretome in response to tumor necrosis factor-alpha (TNF-alpha)-induced insulin resistance. To conduct this study, we comparatively analyzed the media levels of proteins released from L6 skeletal muscle cells. We found 28 TNF-a modulated secretory proteins by using separate filtering methods: Gene Ontology, SignalP, and SecretomeP, as well as the normalized Spectral Index for label-free quantification. Ten of these secretory proteins were increased and 18 secretory proteins were decreased by TNF-a treatment. Using microarray analysis of Zuker diabetic rat skeletal muscle combined with bioinformatics and QPCR, we found a correlation between TNF-alpha-mediated insulin resistance and type 2 diabetes. This novel approach combining analysis of the conditioned secretome and transcriptome has identified several previously unknown, TNF-alpha-dependent secretory proteins, which establish a foothold for research on the different causes of insulin resistance and their relationships with each other.close151

    Proteomic Analysis of Tumor Necrosis Factor-Alpha (TNF-α)-Induced L6 Myotube Secretome Reveals Novel TNF-α-Dependent Myokines in Diabetic Skeletal Muscle

    No full text
    There is a strong possibility that skeletal muscle can respond to irregular metabolic states by secreting specific cytokines. Obesity-related chronic inflammation, mediated by pro-inflammatory cytokines, is believed to be one of the causes of insulin resistance that results in type 2 diabetes. Here, we attempted to identify and characterize the members of the skeletal muscle secretome in response to tumor necrosis factor-alpha (TNF-α)-induced insulin resistance. To conduct this study, we comparatively analyzed the media levels of proteins released from L6 skeletal muscle cells. We found 28 TNF-α modulated secretory proteins by using separate filtering methods: Gene Ontology, SignalP, and SecretomeP, as well as the normalized Spectral Index for label-free quantification. Ten of these secretory proteins were increased and 18 secretory proteins were decreased by TNF-α treatment. Using microarray analysis of Zuker diabetic rat skeletal muscle combined with bioinformatics and Q-PCR, we found a correlation between TNF-α-mediated insulin resistance and type 2 diabetes. This novel approach combining analysis of the conditioned secretome and transcriptome has identified several previously unknown, TNF-α-dependent secretory proteins, which establish a foothold for research on the different causes of insulin resistance and their relationships with each other
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