Abstract：
:Little is known regarding the interplays between the mechanical and molecular bases for vein graft restenosis. We elucidated the stenosis initiation using a high-frequency ultrasonic (HFU) echogenicity platform and estimated the endothelium yield stress from von-Mises stress computation to predict the damage locations in living rats over time. The venous-arterial transition induced the molecular cascades for autophagy and apoptosis in venous endothelial cells (ECs) to cause neointimal hyperplasia, which correlated with the high echogenicity in HFU images and the large mechanical stress that exceeded the yield strength. The ex vivo perfusion of arterial laminar shear stress to isolated veins further confirmed the correlation. EC damage can be rescued by inhibiting autophagy formation using 3-methyladenine (3-MA). Pretreatment of veins with 3-MA prior to grafting reduced the pathological increases of echogenicity and neointima formation in rats. Therefore, this platform provides non-invasive temporal spatial measurement and prediction of restenosis after venous-arterial transition as well as monitoring the progression of the treatments.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Chang YJ,Huang HC,Hsueh YY,Wang SW,Su FC,Chang CH,Tang MJ,Li YS,Wang SH,Shung KK,Chien S,Wu CCdoi
10.1038/srep22147subject
Has Abstractpub_date
2016-02-26 00:00:00pages
22147issn
2045-2322pii
srep22147journal_volume
6pub_type
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