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We began analyzing https://www.nature.com/articles/srep28056, but it redirected us to https://www.nature.com/articles/srep28056. The analysis below is for the second page.

Title[redir]:
Phosphodiesterase 3B (PDE3B) regulates NLRP3 inflammasome in adipose tissue | Scientific Reports
Description:
Activation of inflammation in white adipose tissue (WAT), includes infiltration/expansion of WAT macrophages, contributes pathogenesis of obesity, insulin resistance and metabolic syndrome. The inflammasome comprises an intracellular sensor (NLR), caspase-1 and the adaptor ASC. Inflammasome activation leads to maturation of caspase-1 and processing of IL1β, contributing to many metabolic disorders and directing adipocytes to a more insulin-resistant phenotype. Ablation of PDE3B in WAT prevents inflammasome activation by reducing expression of NLRP3, caspase-1, ASC, AIM2, TNFα, IL1β and proinflammatory genes. Following IP injection of lipopolysaccharide (LPS), serum levels of IL1β and TNFα were reduced in PDE3B−/−mice compared to WT. Activation of signaling cascades, which mediate inflammasome responses, were modulated in PDE3B−/−mice WAT, including smad, NFAT, NFkB and MAP kinases. Moreover, expression of chemokine CCL2, MCP-1 and its receptor CCR2, which play an important role in macrophage chemotaxis, were reduced in WAT of PDE3B−/−mice. In addition, atherosclerotic plaque formation was significantly reduced in the aorta of apoE−/−/PDE3B−/−and LDL-R−/−/PDE3B−/−mice compared to apoE−/−and LDL-R−/−mice, respectively. Obesity-induced changes in serum-cholesterol were blocked in PDE3B−/−mice. Collectively, these data establish a role for PDE3B in modulating inflammatory response, which may contribute to a reduced inflammatory state in adipose tissue.

Matching Content Categories {📚}

  • Education
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Content Management System {📝}

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Custom-built

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {🔍}

pubmed, tissue, reduced, adipose, mice, expression, pdebmice, nlrp, inflammasome, pdeb, google, scholar, cas, fig, protein, insulin, inflammation, increased, wat, levels, activation, ilβ, inflammatory, signaling, pdebwat, cytokines, data, central, proinflammatory, decreased, genes, compared, resistance, serum, cells, cell, nature, macrophages, caspase, macrophage, significantly, regulation, mkp, shown, total, western, glucose, obesity, tnfα, nfat,

Topics {✒️}

nature portfolio akt/dopamine/bdnf/nrf2 trajectories omnia privacy policy pcr reagent kits raf1-s259 inhibitory-site serine-phosphorylation advertising intramural research program real-time quantitative rt-pcr d12492 research diets c-jun n-terminal kinase nature 481 nature 469 nature 386 nature 492 nature 444 nature calcium-sensing receptor regulates ifn-gamma-inducing factor 0/ reprints transforming growth factor-beta affinity-purified anti-pde3b-nt research diets transforming growth factor-β low-dose lps-induced shock extracellular signal-regulated kinase mitogen-activated protein kinase low-frequency exonic variants hfd-fed pde3b−/−mice led quantitative real-time pcr real-time quantitative pcr il-1beta-converting enzyme stress-activated protein kinases camp/pka-signaling regulated direct adipocyte-mediated phenomenon kappa b-beta regulates tgf-beta/smad3 signaling calcium-sensing receptor m2 anti-inflammatory macrophages3 increased camp/pka signaling20 social media media cybernetics reactive oxygen species-sensitive low-density lipoprotein receptor calmodulin-dependent phosphatase increased camp/pka signaling increased camp/pka-signaling increases il-1β secretion pde3b−/−mouse adipose tissue low-fat standard diet anti-inflammatory phenotype observed

Schema {🗺️}

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         headline:Phosphodiesterase 3B (PDE3B) regulates NLRP3 inflammasome in adipose tissue
         description:Activation of inflammation in white adipose tissue (WAT), includes infiltration/expansion of WAT macrophages, contributes pathogenesis of obesity, insulin resistance and metabolic syndrome. The inflammasome comprises an intracellular sensor (NLR), caspase-1 and the adaptor ASC. Inflammasome activation leads to maturation of caspase-1 and processing of IL1β, contributing to many metabolic disorders and directing adipocytes to a more insulin-resistant phenotype. Ablation of PDE3B in WAT prevents inflammasome activation by reducing expression of NLRP3, caspase-1, ASC, AIM2, TNFα, IL1β and proinflammatory genes. Following IP injection of lipopolysaccharide (LPS), serum levels of IL1β and TNFα were reduced in PDE3B−/−mice compared to WT. Activation of signaling cascades, which mediate inflammasome responses, were modulated in PDE3B−/−mice WAT, including smad, NFAT, NFkB and MAP kinases. Moreover, expression of chemokine CCL2, MCP-1 and its receptor CCR2, which play an important role in macrophage chemotaxis, were reduced in WAT of PDE3B−/−mice. In addition, atherosclerotic plaque formation was significantly reduced in the aorta of apoE−/−/PDE3B−/−and LDL-R−/−/PDE3B−/−mice compared to apoE−/−and LDL-R−/−mice, respectively. Obesity-induced changes in serum-cholesterol were blocked in PDE3B−/−mice. Collectively, these data establish a role for PDE3B in modulating inflammatory response, which may contribute to a reduced inflammatory state in adipose tissue.
         datePublished:2016-06-20T00:00:00Z
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      headline:Phosphodiesterase 3B (PDE3B) regulates NLRP3 inflammasome in adipose tissue
      description:Activation of inflammation in white adipose tissue (WAT), includes infiltration/expansion of WAT macrophages, contributes pathogenesis of obesity, insulin resistance and metabolic syndrome. The inflammasome comprises an intracellular sensor (NLR), caspase-1 and the adaptor ASC. Inflammasome activation leads to maturation of caspase-1 and processing of IL1β, contributing to many metabolic disorders and directing adipocytes to a more insulin-resistant phenotype. Ablation of PDE3B in WAT prevents inflammasome activation by reducing expression of NLRP3, caspase-1, ASC, AIM2, TNFα, IL1β and proinflammatory genes. Following IP injection of lipopolysaccharide (LPS), serum levels of IL1β and TNFα were reduced in PDE3B−/−mice compared to WT. Activation of signaling cascades, which mediate inflammasome responses, were modulated in PDE3B−/−mice WAT, including smad, NFAT, NFkB and MAP kinases. Moreover, expression of chemokine CCL2, MCP-1 and its receptor CCR2, which play an important role in macrophage chemotaxis, were reduced in WAT of PDE3B−/−mice. In addition, atherosclerotic plaque formation was significantly reduced in the aorta of apoE−/−/PDE3B−/−and LDL-R−/−/PDE3B−/−mice compared to apoE−/−and LDL-R−/−mice, respectively. Obesity-induced changes in serum-cholesterol were blocked in PDE3B−/−mice. Collectively, these data establish a role for PDE3B in modulating inflammatory response, which may contribute to a reduced inflammatory state in adipose tissue.
      datePublished:2016-06-20T00:00:00Z
      dateModified:2016-06-20T00:00:00Z
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               name:Cardiovascular and Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, USA
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               name:Cardiovascular and Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, USA
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      name:Cardiovascular and Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, USA
      name:Cardiovascular and Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, USA
      name:Cardiovascular and Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, USA
      name:Cardiovascular and Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, USA
      name:Cardiovascular and Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, USA
      name:Cardiovascular and Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, USA
      name:The laboratory of Computational Biology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, USA
      name:Cardiovascular and Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, USA
      name:Cardiovascular and Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, USA
      name:Cardiovascular and Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, USA

External Links {🔗}(388)

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  • mx.zoho.eu
  • mx2.zoho.eu
  • mx3.zoho.eu

Name Servers:

  • josh.ns.cloudflare.com
  • zita.ns.cloudflare.com

CDN Services {📦}

  • Crossref

5.11s.