S100A9 differentially modifies phenotypic states of neutrophils, macrophages, and dendritic cells: implications for atherosclerosis and adipose tissue inflammation. - Wikidata - awgldk - TriplyDB

S100A9 differentially modifies phenotypic states of neutrophils, macrophages, and dendritic cells: implications for atherosclerosis and adipose tissue inflammation.

S100A9 differentially modifies phenotypic states of neutrophils, macrophages, and dendritic cells: implications for atherosclerosis and adipose tissue inflammation.

http://www.wikidata.org/entity/Q34769986

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Surface acoustic waves enhance neutrophil killing of bacteria.Target-selective protein S-nitrosylation by sequence motif recognition Resolution of Inflammation: What Controls Its Onset?S100A8 and S100A9 in cardiovascular biology and disease Genetic and pharmacological modifications of thrombin formation in apolipoprotein e-deficient mice determine atherosclerosis severity and atherothrombosis onset in a neutrophil-dependent manner The apolipoprotein-AI mimetic peptide L4F at a modest dose does not attenuate weight gain, inflammation, or atherosclerosis in LDLR-null mice.Mechanisms of urokinase plasminogen activator (uPA)-mediated atherosclerosis: role of the uPA receptor and S100A8/A9 proteins Changes of dendritic cells and fractalkine in type 2 diabetic patients with unstable angina pectoris: a preliminary report.TLR9 ligands induce S100A8 in macrophages via a STAT3-dependent pathway which requires IL-10 and PGE2.S100A8/A9 (calprotectin) is critical for development of glomerulonephritis and promotes inflammatory leukocyte-renal cell interactions.S100A9: A Potential Biomarker for the Progression of Non-Alcoholic Fatty Liver Disease and the Diagnosis of Non-Alcoholic Steatohepatitis.S100/calgranulins EN-RAGEing the blood vessels: implications for inflammatory responses and atherosclerosis Loss of myeloid related protein-8/14 exacerbates cardiac allograft rejection.Diabetes promotes an inflammatory macrophage phenotype and atherosclerosis through acyl-CoA synthetase 1.S100 calcium binding proteins and ion channels In vivo targeting of inflammation-associated myeloid-related protein 8/14 via gadolinium immunonanoparticles.Myeloid Cell Prostaglandin E2 Receptor EP4 Modulates Cytokine Production but Not Atherogenesis in a Mouse Model of Type 1 Diabetes.Multiple Evolutionary Origins of Ubiquitous Cu2+ and Zn2+ Binding in the S100 Protein Family.S100A12 expression in thoracic aortic aneurysm is associated with increased risk of dissection and perioperative complications.Expression of Calgranulin Genes S100A8, S100A9 and S100A12 Is Modulated by n-3 PUFA during Inflammation in Adipose Tissue and Mononuclear Cells Role of Calprotectin as a Modulator of the IL27-Mediated Proinflammatory Effect on Endothelial Cells.Endothelial acyl-CoA synthetase 1 is not required for inflammatory and apoptotic effects of a saturated fatty acid-rich environment.Functions of S100 proteins.S100A8 and S100A9: DAMPs at the crossroads between innate immunity, traditional risk factors, and cardiovascular disease.Hyperglycemia promotes myelopoiesis and impairs the resolution of atherosclerosis.Novel insights into the role of S100A8/A9 in skin biology.S100 proteins as diagnostic and prognostic markers in colorectal and hepatocellular carcinoma.Molecular biology of atherosclerosis.Neutrophils produce interleukin 17A (IL-17A) in a dectin-1- and IL-23-dependent manner during invasive fungal infection.Review of Rosai-Dorfman Disease: New Insights into the Pathogenesis of This Rare Disorder.Tumor-derived factors modulating dendritic cell function.Calprotectin in rheumatic diseases.UPF1 regulates myeloid cell functions and S100A9 expression by the hnRNP E2/miRNA-328 balance.The role of damage- and pathogen-associated molecular patterns in inflammation-mediated vulnerability of atherosclerotic plaques.Runx2 Deletion in Smooth muscle Cells Inhibits Vascular Osteochondrogenesis and Calcification but not Atherosclerotic Lesion Formation.Association of calprotectin with leukocyte chemotactic and inflammatory mediators following acute aerobic exercise.Targeting the association of calgranulin B (S100A9) with insulin resistance and type 2 diabetes.Biomarkers in COPD: is mortality the Holy Grail?Differential association of S100A9, an inflammatory marker, and p53, a cell cycle marker, expression with epicardial adipocyte size in patients with cardiovascular disease.The role of monocytosis and neutrophilia in atherosclerosis.

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P2860

S100A9 differentially modifies phenotypic states of neutrophils, macrophages, and dendritic cells: implications for atherosclerosis and adipose tissue inflammation.

http://www.wikidata.org/entity/Q34769986

description

2011 nî lūn-bûn

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2011 թվականի մարտին հրատարակված գիտական հոդված

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CIRCULATIONAHA.110.985523

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S100A9 differentially modifies ...... d adipose tissue inflammation.

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Claus Kerkhoff

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Clemens Sorg

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Jay W Heinecke

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Jessica A Hamerman

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Karin E Bornfeldt

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Lev Becker

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Michelle M Averill

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Renee C Leboeuf

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Shelley Barnhart

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Xin Li

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P2860

Loss of S100A9 (MRP14) results in reduced interleukin-8-induced CD11b surface expression, a polarized microfilament system, and diminished responsiveness to chemoattractants in vitro

Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance

Myeloid-related protein-8/14 is critical for the biological response to vascular injury

Inhibition of dendritic cell differentiation and accumulation of myeloid-derived suppressor cells in cancer is regulated by S100A9 protein

Myeloid-related protein 8/14 and the risk of cardiovascular death or myocardial infarction after an acute coronary syndrome in the Pravastatin or Atorvastatin Evaluation and Infection Therapy: Thrombolysis in Myocardial Infarction (PROVE IT-TIMI ...

Platelet expression profiling and clinical validation of myeloid-related protein-14 as a novel determinant of cardiovascular events

Mrp8 and Mrp14 are endogenous activators of Toll-like receptor 4, promoting lethal, endotoxin-induced shock

S100A8 and S100A9 mediate endotoxin-induced cardiomyocyte dysfunction via the receptor for advanced glycation end products

Neutrophils transiently infiltrate intra-abdominal fat early in the course of high-fat feeding.

Calprotectin--a novel marker of obesity.

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1216-1226

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21382888

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atherosclerosis

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