作者: Agnieszka Paradowska-Gorycka , Andrzej Pawlik , Katarzyna Romanowska-Prochnicka , Ewa Haladyj , Damian Malinowski
DOI: 10.1371/JOURNAL.PONE.0160769
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摘要: Background Rheumatoid arthritis (RA) is one of the chronic autoimmune diseases, with genetic and environmental predisposition, synovial angiogenesis considered to be a notable stage in its pathogenesis. Angiogenesis or vascular proliferation has been suggested pivotal mechanism involved both inflammation/immune activation joint invasion destruction. RA may an “angiogenic disease” because it associated active tissue neovascularization. Vascular endothelial growth factor (VEGF) promotes permeability, regulates angiogenesis, cell migration, chemotaxis, capillary hyper permeability therefore development inflammation. VEGF most potent proangiogenic molecule promoting angiogenic phenotype upregulated RA. Objectives The aim study was identify functional variants their possible association expression, susceptibility severity RA. Methods 581 patients 341 healthy individuals were examined for -1154 A/G, -2578 A/C gene polymorphisms by PCR-RFLP method -634 G/C TaqMan SNP genotyping assay. Serum levels controls measured ELISA. Results A/G polymorphism under codominant, recessive (AA+AG vs. GG) dominant (AA AG+GG) models (p = 0.0009; p 0.004; 0.017, respectively). revealed differences case-control distribution recessive, overdominant (all p<0.0001). Furthermore, not correlated Polish population. The genotype-phenotype analysis showed significant between mean value hemoglobin 0.05), additionally they relevated that number women polymorphic allele C lower than wild type -2578A 0.006). significantly higher control groups (both 0,0001). Conclusion Present findings indicated as well protein