本文采用的英格恩产品: RNA-Entranster-invivo

Original Article Regulation of ZNF580 in pathogenesis of ischemic cerebrovascular disease accompanied with upregulation of Smad2 and ADNPYuyu Luo1,2*, Xiaodong Li3*, Gahu Zhala1, Zongming Wan1, Wencheng Zhang1,2

1Department of Clinical Medicine, Logistics University of Chinese People’s Armed Police Force, Tianjin 300309, China; 2Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury Institute of Cardiovascular Disease, Tianjin 300162, China; 3Department of Orthopaedics, Tianjin Third Central Hospital, Tianjin 300070, China.*Equal contributors

Abstract: Ischemic cerebrovascular disease is caused by the reduction or suspension of artery resulting in nerve cell degeneration or necrosis. We conducted the middle cerebral artery occlusion-reperfusion model (MACO) in rats. The reperfusion increased the mRNA and protein level of zinc finger protein 580 (ZNF580). Meanwhile, upregula-tion of transforming growth factor-β (TGF-β), SMAD family member 2 (SMAD2) and activity-dependent neuroprotec-tive protein (ADNP) were also observed. ZNF580 siRNA treatment decreased the expression of Smad2 and ADNP. Furthermore, we also found that a significant increase in the percentage of necrosis cells in MACO. In summary, the results indicated that ZNF580 may regulate ADNP and Smad2 through TGF-β signaling pathway for protecting cerebrum from ischemic cerebrovascular disease.Keywords: MACO, ZNF580, TGF-β, Smad2, ADNP