Shear Stress Inhibits Apoptosis of Ischemic Brain Microvascular Endothelial Cells

International Journal of Molecular Sciences

Shan Tian⁴  Yulong Bai⁴  Lin Yang²  Xinggang Wang³  Yi Wu⁴  Jie Jia⁴  Yulian Zhu⁴  Yong Cheng¹  Pengyue Zhang⁴  Junfa Wu⁴  Nianhong Wang⁴  Guang Xia³  Hua Liao³  Yuling Zhang⁴  Xiafeng Shen⁴  Huixian Yu⁴ 

[1] Department of Cardiology, Zhengzhou Center Hospital, Zhengzhou University, Zhengzhou 450000, China; E-Mails:;Research Center, EYE & ENT Hospital of Fudan University, Shanghai 200031, China; E-Mail:;Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China; E-Mails:;Department of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, China; E-Mails:

关键词: laminar shear stress;    ischemic stroke;    apoptosis;    brain microvascular endothelial cells;   

DOI  :  10.3390/ijms14011412

来源: mdpi

【 摘 要 】

As a therapeutic strategy for ischemic stroke, to restore or increase cerebral blood flow (CBF) is the most fundamental option. Laminar shear stress (LS), as an important force generated by CBF, mainly acts on brain microvascular endothelial cells (BMECs). In order to study whether LS was a protective factor in stroke, we investigated LS-intervented ischemic apoptosis of rat BMECs (rBMECs) through PE Annexin V/7-AAD, JC-1 and Hoechst 33258 staining to observe the membranous, mitochondrial and nuclear dysfunction. Real-time PCR and western blot were also used to test the gene and protein expressions of Tie-2, Bcl-2 and Akt, which were respectively related to maintain membranous, mitochondrial and nuclear norm. The results showed that LS could be a helpful stimulus for ischemic rBMECs survival. Simultaneously, membranous, mitochondrial and nuclear regulation played an important role in this process.

【 授权许可】

CC BY   
© 2013 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland.