Autoantibodies against AT 1 Receptor Contribute to Vascular
Autoantibodies against AT 1 Receptor Contribute to Vascular Aging and Endothelial Cell Senescence Wang Meili, Yin Xiaochen, Zhang Suli, Mao Chenfeng, Cao Ning, Yang Xiaochun, Bian Jingwei, Hao Weiwei, Fan Qian, Liu Huirong 1 Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China. 2 Beijing Key Laboratory of Metabolic Disorders Related Cardiovascular Disease, Capital Medical University, Beijing, China. 3 Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China. 4 Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China. 5 Beijing Anzhen Hospital, Capital Medical University, Beijing, China. Figure 6. AT 1 -AAs from the PAD patients induced HUVECs senescence. A) Representative western blot and quantitative graphs of p 53, p 21 and p 16 INK 4 a expressions in HUVECs treated with n. Ig. Gs, AT 1 -AAs-Ig. Gs or valsartan plus AT 1 -AAs-Ig. Gs for 72 hrs. B) Photographs of typical SA-&#x 003 B 2; -gal-stained HUVECs in the n. Ig. Gs, AT 1 -AAs-Ig. Gs and valsartan+AT 1 -AAs-Ig. Gs groups. Scale bar = 400 &#x 003 BC; m. C) Quantification of Aging and Disease, 2019, 10(5), 1012 -1025. DOI: 10. 14336/AD. 2018. 0919 percentages of SA-&#x 003 B 2; -gal-positive HUVECs of the indicated groups. Data in the graphs were from 3 independent experiments and were expressed as mean &#x 000 B 1; SEM. &#x 0002 A; p &#x 0003 C; 0. 05, &#x 0002 A; p &#x 0003 C; 0. 01, &#x 0002 A; p &#x 0003 C; 0. 001 vs. the n. Ig. Gs group; # p &#x 0003 C; 0. 05, ## p &#x 0003 C; 0. 01 vs. the AT 1 -AAs group.
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