Role of Excessive Autophagy Induced by Mechanical Overload in Vein Graft Neointima Formation: Prediction and Prevention

Ya Ju Chang, Hui Chun Huang, Yuan Yu Hsueh, Shao Wei Wang, Fong Chin Su, Chih Han Chang, Ming Jer Tang, Yi Shuan Li, Shyh Hau Wang, Kirk K. Shung, Shu Chien, Chia Ching Wu

研究成果: Article

5 引文 (Scopus)

摘要

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.

原文English
文章編號22147
期刊Scientific reports
6
DOIs
出版狀態Published - 2016 二月 26

指紋

Neointima
Autophagy
Veins
Transplants
Ultrasonics
Endothelial Cells
Mechanical Stress
Endothelium
Hyperplasia
Pathologic Constriction
Perfusion
Apoptosis
3-methyladenine

All Science Journal Classification (ASJC) codes

  • General

引用此文

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title = "Role of Excessive Autophagy Induced by Mechanical Overload in Vein Graft Neointima Formation: Prediction and Prevention",
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.",
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AU - Wang, Shao Wei

AU - Su, Fong Chin

AU - Chang, Chih Han

AU - Tang, Ming Jer

AU - Li, Yi Shuan

AU - Wang, Shyh Hau

AU - Shung, Kirk K.

AU - Chien, Shu

AU - Wu, Chia Ching

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