alpha mannosidase/uždegimas

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Heterogenic endothelial responses to inflammation: role for differential N-glycosylation and vascular bed of origin.

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BACKGROUND Endothelial cell responses during inflammation are heterogeneous and key for selectivity in how leukocytes hone in on specific sites and why vascular diseases are highly bed specific. However, mechanisms for this specificity remain unclear. RESULTS Here, we exposed human endothelial cells

Neutrophil activation by inflammatory microcrystals of monosodium urate monohydrate utilizes pertussis toxin-insensitive and -sensitive pathways.

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The activation of leukocytes by particulates is a critical event in certain inflammatory syndromes, including acute gout associated with microcrystals of monosodium urate monohydrate. In this study we have evaluated mechanisms of human neutrophil activation by urate crystals. Both

Kujigamberol interferes with pro-inflammatory cytokine-induced expression of and N-glycan modifications to cell adhesion molecules at different stages in human umbilical vein endothelial cells.

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Kujigamberol is the norlabdane compound isolated from Kuji amber and has recently been shown to prevent Ca2+-signal transduction and exert anti-allergy effects in vitro and in vivo. However, the anti-inflammatory activities of kujigamberol remain unclear. In the present study, we investigated the

Effect of anti-inflammatory steroids on the activity of selected lysosomal hydrolases in serum of rats with experimental liver fibrosis.

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Liver fibrosis was produced in rats by subcutaneous injections of carbon tetrachloride. The effect of anti-inflammatory steroids (hydrocortisone, prednisone, dexamethasone) on the activity of serum lysosomal hydrolases (beta-N-acetylglucosaminidase, beta-glucosidase and alpha-mannosidase) was

Endoplasmic reticulum degradation-enhancing α-mannosidase-like protein 1 targets misfolded HLA-B27 dimers for endoplasmic reticulum-associated degradation.

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OBJECTIVE HLA-B27 forms misfolded heavy chain dimers, which may predispose individuals to inflammatory arthritis by inducing endoplasmic reticulum (ER) stress and the unfolded protein response (UPR). This study was undertaken to define the role of the UPR-induced ER-associated degradation (ERAD)

Alpha-mannosidase activity in synovial fluid.

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A microassay technique for the evaluation of synovial fluid alpha-mannosidase activity is presented with the evaluation of 184 synovial fluid samples from a variety of arthropathic conditions. The results indicate a close correlation of enzyme activity with synovial fluid cell count and the degree

Endothelial surface N-glycans mediate monocyte adhesion and are targets for anti-inflammatory effects of peroxisome proliferator-activated receptor γ ligands.

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Endothelial-monocyte interactions are regulated by adhesion molecules and key in the development of vascular inflammatory disease. Peroxisome proliferator-activated receptor (PPAR) γ activation in endothelial cells is recognized to mediate anti-inflammatory effects that inhibit monocyte rolling and

Hydrogen peroxide regulates endothelial surface N-glycoforms to control inflammatory monocyte rolling and adhesion.

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Monocyte extravasation through the endothelial layer is a hallmark of atherosclerotic plaque development and is mediated by heavily N-glycosylated surface adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1). N-glycosylation is a key co- and post-translational modification that

Intestinal Epithelial Cell-specific Deletion of α-Mannosidase II Ameliorates Experimental Colitis.

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Inflammatory bowel disease (IBD) is a refractory disease of the gastrointestinal tract that is believed to develop in genetically susceptible individuals. Glycosylation, a type of post-translational modification, is involved in the development of a wide range of diseases, including IBD, by

Swainsonine, an alpha-mannosidase inhibitor, may worsen cervical cancer progression through the increase in myeloid derived suppressor cells population.

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Cervical cancer, caused by high oncogenic risk Human Papillomavirus (HPV) infection, continues to be a public health problem, mainly in developing countries. Using peptide phage display as a tool to identify potential molecular targets in HPV associated tumors, we identified α-mannosidase, among

Increased activity of lysosomal enzymes in the peritoneal fluid of patients with gynecologic cancers and pelvic inflammatory disease.

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OBJECTIVE To investigate whether the activity of lysosomal enzymes is increased in the peritoneal fluid of patients with gynecologic cancers compared to activity in the peritoneal fluid from normal subjects and those with pelvic inflammatory disease, and fluid from benign ovarian

Mammalian N-glycan branching protects against innate immune self-recognition and inflammation in autoimmune disease pathogenesis.

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Autoimmune diseases are prevalent and often life-threatening syndromes, yet the pathogenic triggers and mechanisms involved remain mostly unresolved. Protein asparagine linked- (N-) glycosylation produces glycan structures that substantially differ among the extracellular compartments of

[Demodex and perifollicular inflammation in man: review and report of 69 biopsies].

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The activities of several lysosomal hydrolases (beta-galactosidase, beta-hexosaminidase, alpha-mannosidase, beta-glycuronidase and acid phosphatase) were determined in serum and blood lymphocytes from patients affected with scleroderma. Statistical comparisons between means of patient and control

Up-regulation of golgi α-mannosidase IA and down-regulation of golgi α-mannosidase IC activates unfolded protein response during hepatocarcinogenesis.

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α-1,2 mannosidases, key enzymes in N-glycosylation, are required for the formation of mature glycoproteins in eukaryotes. Aberrant regulation of α-1,2 mannosidases can result in cancer, although the underlying mechanisms are unclear. Here, we report the distinct roles of α-1,2 mannosidase subtypes

Increased sensitivity of Apolipoprotein E knockout mice to swainsonine dependent immunomodulation.

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The mechanisms that mediate accelerated atherosclerosis in autoimmune diseases remain unclear. One common mechanism that has been documented in autoimmune diseases and atherosclerosis is formation of hypoglycosyalted N-glycans on the cell surface. In this study we tested the effects of swainsonine,

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