title: Role of agonistic autoantibodies against type-1 angiotensin II receptor in the pathogenesis of retinopathy in preeclampsia.
abstract: To investigate the mechanism underlying AT1-AA-induced retinopathy in severe preeclampsia by measuring the positive rate and titer of AT1-AA in plasma from women with severe preeclampsia and normal pregnant women to see whether AT1-AA titer was correlated with the grade of retinopathy. A preeclampsia rat model was also established by intravenous injection of AT1-AA extracted from the plasma of patient suffering from severe preeclampsia. The results showed that the plasma titer and positive rate of AT1-AA were significantly higher in women with severe preeclampsia than normal pregnant women. The antibody titer in cases of severe preeclampsia was associated with the grade of retinopathy, and positively correlated with the level of TNF-α and VEGF. The animal experiment results showed that the modeled rats presented symptoms very similar to symptoms of human preeclampsia, including retinopathy. Ocular fundus examination showed retinal microvascular abnormalities, hemorrhaging and leakage in the severe preeclampsia. Morphological changes included edema, thickening of the INL and ONL, and pigment atrophy. TNF-α and VEGF levels were increased in the vitreous humor and retina of the model rats. Our studies results suggest that abnormal expression of AT1-AA could induce damage to retinal capillary endothelial cells and increase vascular permeability, resulting in retinopathy.
authors.affiliation: Department of Ophthalmology, Shanghai Tenth People's Hospital of Tongji University, 301 Yanchang Rd, Shanghai 200072, China.
authors.forename: Fang
authors.initials: F
authors.lastname: Liu
authors.affiliation: Department of Obstetrics, The First Hospital, Shanxi Medical University, 85 South Jiefang Road, Taiyuan, Shanxi 030001, China.
authors.forename: Yuxian
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Physiology, School of Medicine, Shanghai Jiaotong University, 280 South Chongqing Road, Shanghai 200025, China.
authors.forename: Xiaofang
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Physiology, School of Medicine, Shanghai Jiaotong University, 280 South Chongqing Road, Shanghai 200025, China.
authors.forename: Yanqian
authors.initials: Y
authors.lastname: Zheng
authors.affiliation: Department of Physiology, School of Medicine, Shanghai Jiaotong University, 280 South Chongqing Road, Shanghai 200025, China.
authors.forename: Zhu
authors.initials: Z
authors.lastname: Jin
authors.affiliation: Department of Physiology, School of Medicine, Shanghai Jiaotong University, 280 South Chongqing Road, Shanghai 200025, China.
authors.forename: Jianming
authors.initials: J
authors.lastname: Zhi
mesh_terms: D000328:Adult; D000818:Animals; D001323:Autoantibodies / Q000097:blood / Q000276:immunology*; D005260:Female; D006801:Humans; D058437:Hypertensive Retinopathy / Q000276:immunology* / Q000473:pathology; D011225:Pre-Eclampsia / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D011247:Pregnancy; D051381:Rats; D044140:Receptor, Angiotensin, Type 1 / Q000276:immunology* / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
chemical_list: D001323:Autoantibodies; D044140:Receptor, Angiotensin, Type 1; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A