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Shear Stress Inhibits Apoptosis of Ischemic Brain Microvascular Endothelial Cells

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 protecti...

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Detalles Bibliográficos
Autores principales: Tian, Shan, Bai, Yulong, Yang, Lin, Wang, Xinggang, Wu, Yi, Jia, Jie, Zhu, Yulian, Cheng, Yong, Zhang, Pengyue, Wu, Junfa, Wang, Nianhong, Xia, Guang, Liao, Hua, Zhang, Yuling, Shen, Xiafeng, Yu, Huixian, Hu, Yongshan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3565327/
https://www.ncbi.nlm.nih.gov/pubmed/23344049
http://dx.doi.org/10.3390/ijms14011412
Descripción
Sumario: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.