Advanced glycation end products (AGEs) are a contributing factor in the @entity7499 that is characteristic of proliferative @entity6 . However, a previous study made a promising observation that domain I  -IV of b2  -glycoprotein  I (DI  -IV) inhibits @entity7499 in @entity1 umbilical vein cells. The present study aimed to confirm the inhibition of AGE  -induced @entity7499 in retinal endothelial cells by DI  -IV and to investigate the potential underlying mechanisms. The RF/6A @entity2608 choroid  -retinal vascular endothelial cell line was cultured in  vitro and treated with AGEs in the presence or absence of different concentrations of DI  -IV. The proliferation, migration and tube formation of the RF/6A cells were evaluated using MTS assays, in  vitro wound healing assays and in  vitro Matrigel @entity7499 assays, respectively. The mRNA expression of @entity7 ( @entity7 ), @entity319 ( @entity319 )  2, @entity319  1 and receptor for AGE ( @entity4283 ) were quantified by reverse transcription quantitative polymerase chain reaction. The expression of @entity6758 , @entity319 and the activation of protein kinase B ( @entity584 ) and extracellular signal  -regulated kinase (ERK) were also assessed by western blot analysis. The results indicated that AGEs promoted the migration, proliferation and tube formation of RF/6A cells in  vitro  (P<0.05), increased the expression of @entity7 , @entity319 and @entity4283  (P<0.05) and increased the phosphorylation of @entity584 and ERK (P<0.05). DI  -IV inhibited the increase in @entity319 mRNA and protein, but did not inhibit the increase in @entity7 or @entity4283 mRNAs. These results led to the conclusion that DI  -IV inhibited AGE  -induced @entity7499 in the RF/6A cells, which was accompanied by a downregulation in the expression of @entity319 and its downstream phosphatidylinosol 3  -kinase/ @entity584 and mitogen  -activated protein kinase/ @entity1366  pathways. These findings provide further support towards the treatment of proliferative @entity6 by interventions that act via a mechanism similar to that of DI  -IV.

Domain I-IV of b2-glycoprotein  I inhibits advanced glycation end product-induced XXXX by down-regulating @entity7  2 signaling.

@entity1 :: ('9606', 'Species') :: ['human'] @entity7499 :: ('MESH:D016510', 'Disease') :: ['angiogenesis'] @entity6 :: ('MESH:D003920', 'Disease') :: ['diabetic retinopathy'] @entity7 :: ('7422', 'Gene') :: ['vascular endothelial growth factor', 'VEGF'] @entity6758 :: ('2321', 'Gene') :: ['VEGFR  -1'] @entity584 :: ('207', 'Gene') :: ['Akt'] @entity319 :: ('3791', 'Gene') :: ['VEGFR', 'VEGF receptor', 'VEGFR  -2'] @entity2608 :: ('9544', 'Species') :: ['rhesus macaque'] @entity4283 :: ('177', 'Gene') :: ['RAGE'] @entity1366 :: ('5595;5594', 'Gene') :: ['ERK1/2']
@entity7499 :: (MESH:D016510,Disease) :: ['angiogenesis']
