Low doses of lipopolysaccharide and minimally oxidized low-density lipoprotein cooperatively activate macrophages via nuclear factor kappa B and activator protein-1: possible mechanism for acceleration of atherosclerosis by subclinical endotoxemia
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Fundamental role of pan-inflammation and oxidative-nitrosative pathways in neuropathogenesis of Alzheimer's disease in focal cerebral ischemic ratsFundamental role of pan-inflammation and oxidative-nitrosative pathways in neuropathogenesis of Alzheimer's diseaseOxidation-specific epitopes and immunological responses: Translational biotheranostic implications for atherosclerosisThe SYK side of TLR4: signalling mechanisms in response to LPS and minimally oxidized LDLThe influence of innate and adaptive immune responses on atherosclerosisPathophysiology and Treatments of Oxidative Injury in Ischemic Stroke: Focus on the Phagocytic NADPH Oxidase 2Electronegative LDL: a circulating modified LDL with a role in inflammationModest effect on plaque progression and vasodilatory function in atherosclerosis-prone mice exposed to nanosized TiO(2)Phenotypic modulation of macrophages in response to plaque lipids.Molecular and cellular mechanisms responsible for cellular stress and low-grade inflammation induced by a super-low dose of endotoxinPrimary hyperparathyroidism influences the expression of inflammatory and metabolic genes in adipose tissue.Myeloid IκBα deficiency promotes atherogenesis by enhancing leukocyte recruitment to the plaquesNuclear receptors and inflammation control: molecular mechanisms and pathophysiological relevance.The oxidative stress product carboxyethylpyrrole potentiates TLR2/TLR1 inflammatory signaling in macrophagesSpleen tyrosine kinase regulates AP-1 dependent transcriptional response to minimally oxidized LDLOxidized cholesteryl esters and phospholipids in zebrafish larvae fed a high cholesterol diet: macrophage binding and activation.Network topologies and dynamics leading to endotoxin tolerance and priming in innate immune cells.A strategy to study pathway cross-talks of cells under repetitive exposure to stimuli.Innate immune programing by endotoxin and its pathological consequencesInflammatory stimuli induce inhibitory S-nitrosylation of the deacetylase SIRT1 to increase acetylation and activation of p53 and p65Alteration of lysosome fusion and low-grade inflammation mediated by super-low-dose endotoxin.Cardiovascular complications in inflammatory bowel disease.The influence of calcitonin gene-related peptide on markers of bone metabolism in MG-63 osteoblast-like cells co-cultured with THP-1 macrophage-like cells under virtually osteolytic conditions.Molecular mechanisms responsible for the selective and low-grade induction of proinflammatory mediators in murine macrophages by lipopolysaccharideOxidized LDLs inhibit TLR-induced IL-10 production by monocytes: a new aspect of pathogen-accelerated atherosclerosis.Paying the Toll for Glucose Regulation: A Central Role for TLR3.Triglyceride-Rich Lipoproteins Modulate the Distribution and Extravasation of Ly6C/Gr1(low) Monocytes.microRNA-181a represses ox-LDL-stimulated inflammatory response in dendritic cell by targeting c-Fos.Molecular mechanisms responsible for the reduced expression of cholesterol transporters from macrophages by low-dose endotoxinLow-grade inflammatory polarization of monocytes impairs wound healingVaricose Remodeling of Veins Is Suppressed by 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitors.Insulin-Like Growth Factor-1 Receptor Deficiency in Macrophages Accelerates Atherosclerosis and Induces an Unstable Plaque Phenotype in Apolipoprotein E-Deficient Mice.A starring role for stellate cells in the pancreatic cancer microenvironment.Epidemiology, risk factors, and the promotion of pancreatic cancer: role of the stellate cell.Immunometabolism in obese asthmatics: are we there yet?mRNA-binding protein ZFP36 is expressed in atherosclerotic lesions and reduces inflammation in aortic endothelial cellsCationic peptide mR18L with lipid lowering properties inhibits LPS-induced systemic and liver inflammation in ratsThe persistence of low-grade inflammatory monocytes contributes to aggravated atherosclerosis.Toll like receptor (TLR)-4 as a regulator of peripheral endogenous opioid-mediated analgesia in inflammation.A physical interaction between the adaptor proteins DOK3 and DAP12 is required to inhibit lipopolysaccharide signaling in macrophages.
P2860
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P2860
Low doses of lipopolysaccharide and minimally oxidized low-density lipoprotein cooperatively activate macrophages via nuclear factor kappa B and activator protein-1: possible mechanism for acceleration of atherosclerosis by subclinical endotoxemia
description
2010 nî lūn-bûn
@nan
2010 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի մայիսին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Low doses of lipopolysaccharid ...... sis by subclinical endotoxemia
@ast
Low doses of lipopolysaccharid ...... sis by subclinical endotoxemia
@en
type
label
Low doses of lipopolysaccharid ...... sis by subclinical endotoxemia
@ast
Low doses of lipopolysaccharid ...... sis by subclinical endotoxemia
@en
prefLabel
Low doses of lipopolysaccharid ...... sis by subclinical endotoxemia
@ast
Low doses of lipopolysaccharid ...... sis by subclinical endotoxemia
@en
P2093
P2860
P1433
P1476
Low doses of lipopolysaccharid ...... sis by subclinical endotoxemia
@en
P2093
Ayelet Gonen
Christopher Benner
Christopher K Glass
Cody J Diehl
Felicidad Almazan
Philipp Wiesner
Soo-Ho Choi
Susan Butler
Wendy Huang
Yury I Miller
P2860
P356
10.1161/CIRCRESAHA.110.218420
P577
2010-05-20T00:00:00Z