OBJECTIVE: To investigate the role of autoantibodies against @entity2231 ( @entity2231 ) in @entity1 with @entity1252 ( @entity1252 )-associated @entity120 ( @entity120 ) and to examine the possibility that the pathogenesis of this disease is mediated by these autoantibodies. METHODS: @entity2231 autoantibodies in serum from @entity1 with @entity1252 -associated @entity120 and serum from controls ( @entity1252 @entity1 without @entity120 ) were detected via a @entity1 @entity2231 epitope peptide-based enzyme-linked immunosorbent assay. An exploratory cohort of @entity1 with @entity1252 -associated @entity120 (n   =   76) and an independent validation cohort of @entity1 with @entity1252 -associated @entity120 confirmed by right-sided heart catheterization (RHC) (n   =   82) were enrolled. The clinical relevance of @entity2231 autoantibodies in @entity1252 -associated @entity120 was analyzed. The proliferation of vascular smooth muscle cells (SMCs) and the permeability of endothelial cells (ECs) were assessed in vitro in cells stimulated with polyclonal @entity2231 IgG autoantibodies. Expression of @entity120 -related markers, i.e., @entity750 transporter, platelet-derived growth factor receptor b, @entity7 was measured by quantitative polymerase chain reaction. In addition, a suboptimal dose of @entity6560 was used to induce @entity120 in @entity35 , and the effect of @entity2231 autoantibodies in vivo was determined using a @entity8158 index, pulmonary angiography, and laboratory parameters. RESULTS: @entity2231 autoantibodies occurred more frequently in @entity1252 -associated @entity120 (41.5%) than in controls (17.1%). There was a significant correlation between @entity2231 autoantibody titers and pulmonary artery systolic pressure measured by echocardiography (r   =   0.2978, P   =   0.0038) or pulmonary artery systolic pressure measured by RHC (r   =   0.2159, P   =   0.0257) in @entity1252 -associated @entity120 . @entity2231 autoantibodies could promote SMC proliferation, disrupt the endothelial barrier, and up-regulate expression of @entity120 -related markers, which could be blocked in the presence of an endothelin receptor antagonist. @entity2231 autoantibodies aggravated @entity8158 and vascular remodeling in vivo. CONCLUSION: We identified @entity2231 autoantibodies as a biomarker of mechanistic relevance in @entity1252 . These autoantibodies may mediate @entity120 development in @entity1252 .

Anti- XXXX Autoantibodies in @entity1252 Erythematosus-Associated Pulmonary Arterial Hypertension.

@entity1 :: ('9606', 'Species') :: ['human', 'patients'] @entity7 :: ('7422', 'Gene') :: ['vascular endothelial growth factor A, and platelet-derived growth factor B'] @entity6560 :: ('MESH:D016686', 'Chemical') :: ['monocrotaline'] @entity120 :: ('MESH:D006976', 'Disease') :: ['PAH', 'pulmonary arterial hypertension'] @entity1252 :: ('MESH:D008180', 'Disease') :: ['SLE', 'systemic lupus erythematosus'] @entity8158 :: ('MESH:D017380', 'Disease') :: ['right ventricular hypertrophy'] @entity750 :: ('MESH:D012701', 'Chemical') :: ['serotonin'] @entity35 :: ('10116', 'Species') :: ['rats'] @entity2231 :: ('1909', 'Gene') :: ['ETRA', 'endothelin 1 receptor type A']
@entity2231 :: (1909,Gene) :: ['Endothelin Receptor Type A']
