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American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 10/2007, Volume 293, Issue 4, pp. 2210 - 2218
Targeting cannabinoid-2 (CB2) receptors with selective agonists may represent a novel therapeutic avenue in various inflammatory diseases, but the mechanisms... 
Adhesion molecules | Inflammation | RhoA | Endothelial activation | C-REACTIVE PROTEIN | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | MOLECULE EXPRESSION | ATHEROSCLEROSIS | NECROSIS-FACTOR-ALPHA | KNOCKOUT MICE | endothelial activation | CANNABINOID RECEPTORS | inflammation | adhesion molecules | NITRIC-OXIDE | THERAPEUTIC TARGETS | PERIPHERAL VASCULAR DISEASE | POTENTIAL ROLE | CB2 RECEPTOR ACTIVATION | Inflammation - chemically induced | Leukocyte Rolling - drug effects | Tumor Necrosis Factor-alpha - metabolism | Receptor, Cannabinoid, CB2 - agonists | Humans | Male | Monocytes - metabolism | NF-kappa B - metabolism | rhoA GTP-Binding Protein - metabolism | Aorta - metabolism | RNA, Messenger - metabolism | Receptor, Cannabinoid, CB2 - genetics | Coronary Vessels - metabolism | Lipopolysaccharides | Dose-Response Relationship, Drug | Inflammation - metabolism | Anti-Inflammatory Agents - therapeutic use | Chemokine CCL2 - metabolism | Disease Models, Animal | Coronary Vessels - drug effects | Anti-Inflammatory Agents - pharmacology | Endothelial Cells - metabolism | Aorta - drug effects | Mice, Inbred C57BL | Cells, Cultured | Cannabinoids - pharmacology | Monocytes - drug effects | Receptor, Cannabinoid, CB1 - metabolism | Receptor, Cannabinoid, CB2 - metabolism | Cannabinoids - therapeutic use | Intercellular Adhesion Molecule-1 - metabolism | Animals | Signal Transduction - drug effects | Inflammation - prevention & control | Mice | Vascular Cell Adhesion Molecule-1 - metabolism | Endothelial Cells - drug effects
Journal Article
Journal of gastroenterology and hepatology, ISSN 0815-9319, 03/2009, Volume 24, Issue 3, pp. 443 - 452
Background and Aims:  We examined extrinsic and intrinsic (endogenous) mitochondrial apoptosis pathways in experimental non‐alcoholic steatohepatitis (NASH).... 
mitochondria | methionine and choline deficiency | insulin‐like growth factor‐1 | TRAIL‐R killer/DR5 | TNF receptors | cell death pathways | p53 | Cell death pathways | TRAIL-R killer/DR5 | Methionine and choline deficiency | Mitochondria | Insulin-like growth factor-1 | P53 | HEPATOCYTE APOPTOSIS | ACIDS | DR5 | insulin-like growth factor-1 | NONALCOHOLIC STEATOHEPATITIS | LIVER-DISEASE | PATHOGENESIS | NECROSIS | TNF-ALPHA | LIGAND | GASTROENTEROLOGY & HEPATOLOGY | TRAIL-R killer | NF-KAPPA-B | HEPATIC STEATOSIS | Liver - pathology | Liver - enzymology | Fatty Liver - pathology | Mitochondria, Liver - metabolism | Caspase 3 - metabolism | Choline Deficiency - complications | Male | Alanine Transaminase - blood | Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism | Receptors, Tumor Necrosis Factor, Type I - metabolism | RNA, Messenger - metabolism | fas Receptor - metabolism | Tumor Suppressor Protein p53 - genetics | Time Factors | Receptors, Tumor Necrosis Factor, Type II - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Nutritional Status | Receptors, TNF-Related Apoptosis-Inducing Ligand - genetics | BH3 Interacting Domain Death Agonist Protein - metabolism | Disease Models, Animal | Methionine - deficiency | Receptors, Tumor Necrosis Factor - metabolism | Fatty Liver - metabolism | Mitochondria, Liver - pathology | Liver - metabolism | Mice, Inbred C57BL | Gene Expression Regulation | Tumor Suppressor Protein p53 - metabolism | Mitochondria, Liver - enzymology | Animals | Mice | bcl-X Protein - metabolism | Insulin-Like Growth Factor I - metabolism | Apoptosis | Fatty Liver - etiology | BH3 Interacting Domain Death Agonist Protein, metabolism | Receptors, Tumor Necrosis Factor, Type II, metabolism | Fatty Liver, pathology | Mitochondria, Liver, metabolism | Receptors, Tumor Necrosis Factor, metabolism | Cyclin-Dependent Kinase Inhibitor p21, metabolism | Insulin-Like Growth Factor I, metabolism | Caspase 3, metabolism | Antigens, CD95, metabolism | RNA, Messenger, metabolism | Tumor Suppressor Protein p53, metabolism | Methionine, deficiency | Choline Deficiency, complications | Tumor Suppressor Protein p53, genetics | bcl-X Protein, metabolism | Mitochondria, Liver, pathology | Liver, pathology | Alanine Transaminase, blood | Liver, metabolism | Fatty Liver, metabolism | Receptors, TNF-Related Apoptosis-Inducing Ligand, metabolism | Liver, enzymology | Fatty Liver, etiology | Mitochondria, Liver, enzymology | Receptors, Tumor Necrosis Factor, Type I, metabolism | Receptors, TNF-Related Apoptosis-Inducing Ligand, genetics | Messenger RNA | Choline | Methionine | Mitochondrial DNA | Tumor proteins | Peptide hormones | Growth factors
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 08/2007, Volume 293, Issue 2, pp. 909 - 918
Recent studies have uncovered important cross talk between inflammation, generation of reactive oxygen and nitrogen species, and lipid metabolism in the pathogenesis of cardiovascular aging... 
Pressure-volume relationship | Cardiac function | Endocannabinoids | Anandamide | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | ANANDAMIDE HYDROLYSIS | HEART-FAILURE | ENDOGENOUS CANNABINOID SYSTEM | ENDOCANNABINOID SYSTEM | RECEPTOR | KNOCKOUT MICE | CORONARY-ARTERIES | HEMODYNAMIC PROFILE | pressure-volume relationship | NITRIC-OXIDE | PERIPHERAL VASCULAR DISEASE | cardiac function | endocannabinoids | VASCULAR ENDOTHELIAL-CELLS | anandamide | Tumor Necrosis Factor-alpha - metabolism | Inflammation - pathology | Humans | Monocytes - metabolism | NF-kappa B - metabolism | Coronary Vessels - metabolism | Receptors, Cannabinoid - metabolism | Arachidonic Acids - metabolism | Inflammation - metabolism | Aging - genetics | Ventricular Dysfunction, Left - genetics | Myocardium - metabolism | Ventricular Dysfunction, Left - pathology | Ventricular Dysfunction, Left - enzymology | Amidohydrolases - deficiency | Amidohydrolases - metabolism | Endothelial Cells - metabolism | Reactive Nitrogen Species - metabolism | Amidohydrolases - genetics | Cells, Cultured | Gene Expression Regulation | Polyunsaturated Alkamides - metabolism | Cell Adhesion | Aging - pathology | Mice, Knockout | Ventricular Dysfunction, Left - metabolism | Intercellular Adhesion Molecule-1 - metabolism | Myocardium - enzymology | Animals | Coronary Vessels - cytology | Inflammation - genetics | Mice | Vascular Cell Adhesion Molecule-1 - metabolism | Inflammation - enzymology | Aging - metabolism | Apoptosis
Journal Article
The Journal of immunology (1950), ISSN 0022-1767, 01/2014, Volume 192, Issue 2, pp. 623 - 629
.... Although the precise origin of the unchecked inflammatory response in obesity is unclear, it is known that overproduction of proinflammatory cytokines by innate immune cells affects metabolism... 
IMMUNE-SYSTEM | INFLAMMATION | DISEASE | RESISTANCE | FAT | AKT | IMMUNOLOGY | DIET-INDUCED OBESITY | KEY PLAYERS | ADIPOSE-TISSUE | CUTTING EDGE | Tumor Necrosis Factor-alpha - metabolism | Antigens, CD - immunology | T-Lymphocytes, Regulatory - metabolism | Epithelial Cells - metabolism | TOR Serine-Threonine Kinases - metabolism | Obesity - immunology | Insulin - immunology | Interferon-gamma - metabolism | Antigens, CD - metabolism | T-Lymphocytes, Regulatory - immunology | Epithelium - immunology | Signal Transduction - immunology | Inflammation - metabolism | Tumor Necrosis Factor-alpha - immunology | Interleukin-10 - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Receptor, Insulin - immunology | Macrophages - immunology | Hyperinsulinism - metabolism | Intra-Abdominal Fat - immunology | Transforming Growth Factor beta - immunology | Epithelium - metabolism | Mice, Inbred C57BL | Apyrase - metabolism | Cells, Cultured | Apyrase - immunology | CTLA-4 Antigen - metabolism | Inflammation - immunology | CTLA-4 Antigen - immunology | Intra-Abdominal Fat - metabolism | Obesity - metabolism | TOR Serine-Threonine Kinases - immunology | Insulin - metabolism | Macrophages - metabolism | Animals | Hyperinsulinism - immunology | Proto-Oncogene Proteins c-akt - immunology | Epithelial Cells - immunology | Interferon-gamma - immunology | Interleukin-10 - antagonists & inhibitors | Receptor, Insulin - metabolism | Mice | Interleukin-10 - immunology | Transforming Growth Factor beta - metabolism
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2010, Volume 107, Issue 28, pp. 12611 - 12616
Asbestos carcinogenesis has been linked to the release of cytokines and mutagenic reactive oxygen species (ROS) from inflammatory cells. Asbestos is cytotoxic... 
Actinomycin | Asbestos | Cell death | Secretion | Plasma cells | Inflammation | Macrophages | Carcinogenesis | Necrosis | Apoptosis | Mesothelioma | Biomarker | Tumor necrosis factor-alpha | Chemoprevention | TRANSFORMATION | POLY(ADP-RIBOSE) POLYMERASE | MACROPHAGES | MULTIDISCIPLINARY SCIENCES | CROCIDOLITE ASBESTOS | HMGB1 | biomarker | MAMMALIAN-CELLS | tumor necrosis factor-alpha | PATHOGENESIS | chemoprevention | NECROTIC CELLS | carcinogenesis | TNF-ALPHA | INHIBITORS | mesothelioma | Tumor Necrosis Factor-alpha - metabolism | Asbestos - metabolism | Epithelial Cells - metabolism | Reactive Oxygen Species - metabolism | Humans | Reactive Oxygen Species - pharmacology | Adenosine Diphosphate Ribose - metabolism | Adenosine Diphosphate Ribose - pharmacology | Carcinogens - metabolism | Asbestos - pharmacology | Pleural Neoplasms - metabolism | Inflammation - metabolism | Carcinogens - pharmacology | Cell Nucleus - metabolism | HMGB Proteins - pharmacology | HMGB1 Protein - pharmacology | HMGB1 Protein - metabolism | Cell Death | Mesocricetus | Female | HMGB Proteins - metabolism | Poly Adenosine Diphosphate Ribose - pharmacology | Epithelium - drug effects | Cricetinae | Cytokines - metabolism | Epithelium - metabolism | Hydrogen Peroxide - pharmacology | Necrosis - metabolism | Hydrogen Peroxide - metabolism | Tumor Necrosis Factor-alpha - pharmacology | Macrophages - metabolism | Poly(ADP-ribose) Polymerases - metabolism | Animals | Mesothelioma - metabolism | Poly(ADP-ribose) Polymerases - pharmacology | Cells - metabolism | Mice | Mice, Inbred BALB C | Cytokines - pharmacology | Prevention | Mesothelium | Chromosomal proteins | Research | Chemical properties | Health aspects | Reactive oxygen species | Transformation | Deposits | Hydrogen peroxide | Cytokines | Cytotoxicity | HMGB1 protein | Nuclei | Carcinogens | Tumor necrosis factor-a | ATP | Cytoplasm | Biological Sciences
Journal Article
Journal of Vascular Surgery, ISSN 0741-5214, 2015, Volume 64, Issue 5, pp. 1444 - 1449
Journal Article
Nature (London), ISSN 1476-4687, 2011, Volume 471, Issue 7340, pp. 637 - 641
Journal Article
Molecular and cellular biology, ISSN 0270-7306, 2003, Volume 23, Issue 4, pp. 1428 - 1440
Journal Article
Journal Article
Arthritis research & therapy, ISSN 1478-6354, 2013, Volume 15, Issue 5, pp. R151 - R151
Introduction: T helper (Th)-17 cells are increased in systemic sclerosis (SSc). We therefore assessed whether Th17 cells could modulate the inflammatory and... 
RHEUMATOID-ARTHRITIS | MATRIX METALLOPROTEINASES | SYNOVIAL FIBROBLASTS | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | GENE-EXPRESSION | SKIN FIBROSIS | NECROSIS-FACTOR-ALPHA | RHEUMATOLOGY | NF-KAPPA-B | T-CELLS | PULMONARY-FIBROSIS | Interleukin-8 - genetics | Gene Expression - drug effects | Skin - metabolism | Humans | Scleroderma, Systemic - pathology | Culture Media, Conditioned - pharmacology | Male | Interleukin-17 - pharmacology | Dose-Response Relationship, Drug | Collagen Type I - genetics | Th17 Cells - metabolism | Radioimmunoassay | Inflammation Mediators - metabolism | Female | Chemokine CCL2 - metabolism | Interleukin-8 - metabolism | Matrix Metalloproteinase 1 - genetics | Skin - pathology | Fibroblasts - metabolism | Collagen Type I - metabolism | Enzyme-Linked Immunosorbent Assay | Scleroderma, Systemic - metabolism | Cells, Cultured | Scleroderma, Systemic - genetics | Chemokine CCL2 - genetics | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Tumor Necrosis Factor-alpha - pharmacology | Fibroblasts - drug effects | Matrix Metalloproteinase 1 - metabolism | Interferon-gamma - pharmacology | Culture Media, Conditioned - metabolism | Proteins | Medical equipment and supplies industry | Interleukins | Systemic scleroderma | Medical test kit industry | Scleroderma (Disease) | High-definition television | Skin | Biological response modifiers | Enzyme-linked immunosorbent assay
Journal Article
Gastroenterology (New York, N.Y. 1943), ISSN 0016-5085, 2011, Volume 141, Issue 2, pp. 621 - 632
Background & Aims Epithelial cells that cover the intestinal mucosal surface maintain immune homeostasis and tolerance in the gastrointestinal tract. However,... 
Gastroenterology and Hepatology | IgA | Inflammatory Bowel Disease | T Cell | Immune Response | CELLS | COMPLEX | ACTIVATION | POLYMERIC IMMUNOGLOBULIN RECEPTOR | INTESTINAL EPITHELIUM | TRANSPORT | INFLAMMATORY-BOWEL-DISEASE | ADAPTER | HOST-DEFENSE | INFECTION | GASTROENTEROLOGY & HEPATOLOGY | Tumor Necrosis Factor-alpha - metabolism | Intestinal Mucosa - metabolism | Adaptor Protein Complex mu Subunits - metabolism | Epithelial Cells - metabolism | Adaptor Protein Complex beta Subunits - deficiency | Humans | Cell Membrane Permeability | Crohn Disease - metabolism | Cell Membrane - physiology | Ribonucleases - metabolism | Adaptor Protein Complex 1 - metabolism | Th17 Cells - metabolism | Intestinal Mucosa - immunology | alpha-Defensins - metabolism | Adaptor Protein Complex beta Subunits - immunology | Cell Membrane - metabolism | beta-Defensins - metabolism | Colon | Receptors, Cytokine - metabolism | Colitis - immunology | Adaptor Protein Complex 1 - deficiency | Lipocalins - metabolism | Adaptor Protein Complex 1 - immunology | Immunoglobulin A - metabolism | Signal Transduction | Acute-Phase Proteins - metabolism | Down-Regulation | Oncogene Proteins - metabolism | Homeostasis - immunology | Epithelial Cells - pathology | S100 Proteins - metabolism | Muramidase - metabolism | Intestinal Mucosa - microbiology | Mice, Knockout | Interleukin-17 - metabolism | Adaptor Protein Complex beta Subunits - metabolism | Animals | Colitis - microbiology | Proteins - metabolism | Ribonuclease, Pancreatic - metabolism | Lipocalin-2 | Cathelicidins - metabolism | Epithelial Cells - immunology | Receptors, Cytokine - immunology | Mice | Intestinal Mucosa - pathology | Medical colleges | Fc receptors | Gastrointestinal diseases | Homeostasis | Biological response modifiers | Immunoglobulin A | T cells
Journal Article
Journal of hepatology, ISSN 0168-8278, 2011, Volume 54, Issue 4, pp. 795 - 809
The unfolded protein response (UPR) is activated upon the accumulation of misfolded proteins in the endoplasmic reticulum (ER) that are sensed by the binding... 
Gastroenterology and Hepatology | Hepatosteatosis | Endoplasmic reticulum stress | Unfolded protein response | Liver injury | MESSENGER-RNA TRANSLATION | UNFOLDED-PROTEIN RESPONSE | TRANSCRIPTION FACTOR XBP-1 | NECROSIS-FACTOR-ALPHA | ISCHEMIA-REPERFUSION INJURY | PROGRAMMED CELL-DEATH | GLUCOSE-REGULATED PROTEINS | HEPATITIS-C VIRUS | HUMAN HEPATOCELLULAR-CARCINOMA | GASTROENTEROLOGY & HEPATOLOGY | NF-KAPPA-B | Hepatitis C, Chronic - metabolism | Fatty Liver - metabolism | Cholestasis - metabolism | eIF-2 Kinase - metabolism | Humans | Liver Diseases - pathology | Stress, Physiological | Endoplasmic Reticulum - metabolism | Hyperhomocysteinemia - metabolism | Hepatocytes - pathology | Hepatocytes - metabolism | Unfolded Protein Response | Liver Diseases, Alcoholic - metabolism | Activating Transcription Factor 6 - metabolism | Inflammation - metabolism | Animals | Models, Biological | Liver Neoplasms - metabolism | Non-alcoholic Fatty Liver Disease | Protein Conformation | Liver Diseases - metabolism | Reperfusion Injury - metabolism | Apoptosis | Carcinoma, Hepatocellular - metabolism | Inositol | Immunoglobulins | Stress (Physiology) | Ribonuclease | Glucose | Genetic translation | Dextrose | Messenger RNA | Proteases | Proteolysis | Analysis | Hepatitis C | Adenylic acid | Hepatitis C virus | Health aspects | Protein binding | Tumors
Journal Article