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Evidence indicating an important link between glycosylation changes and autoimmune rheumatic disease is presented. Attention is especially focused on the interrelationship between reduced galactosylation of the oligosaccharides of IgG, auto-sensitization which is thought to be of central importance in the pathogenesis of rheumatoid arthritis (RA), and the enzyme 1,4-galactosyltransferase (GTase) that catalyses the addition of galactose to the oligosaccharide chains on this molecule. Data are presented to indicate that GTase undergoes a variety of normal and disease associated changes. These variations are believed to contribute to the pathological processes in rheumatoid disease, and a hypothesis is suggested, whereby disease is associated with the dysregulation of an integrated glycosylation network, comprising IgG galactosylation, lymphocytic GTase and anti-GTase antibodies, that is a component of the normal immune system. 相似文献
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Elyasi Far Babak Yari Khosroushahi Ahmad Dilmaghani Azita 《International journal of peptide research and therapeutics》2020,26(4):2241-2251
International Journal of Peptide Research and Therapeutics - Protease is a kind of enzyme with different applications in medicine and industry. The limitation of the enzymes in industry is lack of... 相似文献
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Jacobson A Yan C Gao Q Rincon-Skinner T Rivera A Edwards J Huang A Kaley G Sun D 《American journal of physiology. Heart and circulatory physiology》2007,293(3):H1344-H1350
The purpose of this study was to investigate the mechanisms that regulate superoxide (O(2)(*-)) production as a function of an acute elevation of intravascular pressure and age. Mesenteric arteries isolated from young (6 mo) and aged (24 mo) male Fischer 344 rats were used. O(2)(*-) production in vessels in response to 80 (normal pressure, NP) and 180 (high pressure, HP) mmHg was determined by the superoxide dismutase-inhibitable nitroblue tetrazolium (NBT) reduction assay. In vessels exposed to NP, O(2)(*-) production was significantly higher in aged than in young vessels (32.7 +/- 7.0 vs. 15.4 +/- 2.4 nmol.mg(-1).30 min(-1)). HP enhanced O(2)(*-) production in vessels of both groups, but the enhancement was significantly greater in aged than in young vessels (63.4 +/- 6.7 vs. 32.7 +/- 4.3 nmol.mg(-1).30 min(-1)). Apocynin (100 micromol/l) attenuated HP-induced increases in O(2)(*-) production in both groups, whereas allopurinol (100 micromol/l) and N(omega)-nitro-L-arginine methyl ester (100 mumol/l) inhibited the response only in aged vessels. Confocal microscopy showed increases in O(2)(*-) in response to HP in endothelial and smooth muscle layers of both groups, with much greater fluorescent staining in aged than in young rats and in the endothelium than in smooth muscle cells. No significant changes in NAD(P)H oxidase gene and protein expressions were observed in vessels of the two groups. Upregulation of protein expression of xanthine oxidase was detected in aged vessels. We conclude that NAD(P)H oxidase contributes importantly to HP-induced enhanced O(2)(*-) production in vessels of both young and aged rats, whereas xanthine oxidase and nitric oxide synthase-dependent O(2)(*-) production also contribute to the enhancement in mesenteric arteries of aged rats. 相似文献
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Azita Monazzam Pasha Razifar Martin Simonsson Fredrik Qvarnström Raymond Josephsson Carl Blomqvist Bengt Långström Mats Bergström 《Cancer cell international》2006,6(1):1-8