Effect of shear stress and substrate on endothelial DAPK expression, caspase activity, and apoptosis

Rennier, Keith; Ji, Julie Y.

doi:10.1186/1756-0500-6-10

Cited by 26 publications

(16 citation statements)

References 39 publications

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“…17 Altering the flow shear stress and wall stress in the arterial wall are well known to stimulate vascular cell functions, including cell proliferation and apoptosis. 12, 21, 34, 36 Our simulation demonstrated significant changes in wall stresses in buckled arteries post-grafting, especially in axial stress (Fig. 8c).…”

Section: Discussionmentioning

confidence: 71%

An In Vivo Rat Model of Artery Buckling for Studying Wall Remodeling

2014

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Theoretical modeling and in vitro experiments have demonstrated that arterial buckling is a possible mechanism for the development of artery tortuosity. However, there has been no report of whether artery buckling develops into tortuosity, partially due to the lack of in vivo models for long-term studies. The objective of this study was to establish an in vivo buckling model in rat carotid arteries for studying arterial wall remodeling after buckling. Rat left carotid arteries were transplanted to the right carotid arteries to generate buckling under in vivo pressure and were maintained for 1 week to examine wall remodeling and adaptation. Our results showed that a significant buckling was achieved in the carotid arterial grafts with altered wall stress. Cell proliferation and matrix metalloprotinease-2 (MMP-2) expression in the buckled arteries increased significantly compared with the controls. The tortuosity level of the grafts also slightly increased 1 week post-surgery, while there was no change in vessel dimensions, blood pressure, and blood flow velocity. The artery buckling model provides a useful tool for further study of the adaptation of arteries into tortuous shapes.

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Section: Discussionmentioning

confidence: 71%

An In Vivo Rat Model of Artery Buckling for Studying Wall Remodeling

2014

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“…DAPK is upstream of the caspases, with the exception of caspase 8, and may induce caspase-independent cell death or autophagy. Previous studies have determined that DAPK contributed to shear stress-induced endothelial apoptosis (20,21). However, the importance of DAPK in Hcy-induced apoptosis in endothelial cells remains to be fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of DAPK contributes to homocysteine-induced endothelial apoptosis via the modulation of Bcl2/Bax and activation of caspase 3

Tian

Shi

Liu

et al. 2016

Molecular Medicine Reports

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Hyperhomocysteinemia is characterized by an abnormally high level of homocysteine (Hcy) in the blood and is associated with cardiovascular diseases such as atherosclerosis. Endothelial dysfunction may lead to the pro-atherogenic effects associated with hyperhomocysteinemia. Endothelial dysfunction induced by Hcy has been previously investigated; however, the underlying molecular mechanism remains to be fully elucidated. The present study investigated whether death-associated protein kinase (DAPK) is involved in Hcy-induced apoptosis in human umbilical vein endothelial cells (HUVECs). It was determined that Hcy treatment upregulated the mRNA and protein expression levels of DAPK in HUVECs. Additionally, it was identified that the knockdown of DAPK using small interfering RNA may attenuate the Hcy-induced apoptosis and dissipation of mitochondrial membrane potential. DAPK inhibition may also reverse the effect of Hcy by the upregulation of B cell leukemia/lymphoma 2 (Bcl2) and poly ADP-ribose polymerase, and the downregulation of Bcl2-associated X protein (Bax) and of caspase 3. In conclusion, the present study demonstrated that DAPK contributed to the Hcy-induced endothelial apoptosis via modulation of Bcl2/Bax expression levels and activation of caspase 3.

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“…Some investigators have cultured vascular cells on 3D collagen scaffolds within their flow chambers to more accurately reproduce the in vivo substrate conditions [32,36]. Rennier and Ji found similar EC response to steady FSS (as indicated by DAPK expression and apoptosis) regardless of whether the cells were cultured on glass or silicone [28]. However, that does not rule out the potential importance of substrate stiffness on cell response.…”

Section: Introductionmentioning

confidence: 93%

“…In the past, most parallel-plate flow chambers have used glass or rigid glasslike materials as a substrate for cell culture [13,18,33,34]. For cells to attach to a rigid substrate, researchers must coat the substrate with fibronectin, collagen, or gelatin [12,18,28,35], or allow the cells time to lay down their own matrix [13]. Rennier and Ji demonstrated that fibronectin-coated silicone membranes (similar to those used for Fig.…”

Section: Introductionmentioning

confidence: 97%

“…FSS as high as 85 dynes/cm 2 has been applied to cells using parallel-plate methods [13]. Other modifications to traditional parallel-plate flow chambers include a temperaturecontrolled stainless steel flow chamber [26] and the use of reservoirs upstream and downstream of the flow channel to promote steady laminar flow [9,27,28]. To generate disturbed flow, the parallel-plate flow chamber can be modified to a "step-flow" channel.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Device-Based In Vitro Techniques for Mechanical Stimulation of Vascular Cells: A Review

Davis

Zambrano

Anumolu

et al. 2015

Journal of Biomechanical Engineering

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The most common cause of death in the developed world is cardiovascular disease. For decades, this has provided a powerful motivation to study the effects of mechanical forces on vascular cells in a controlled setting, since these cells have been implicated in the development of disease. Early efforts in the 1970 s included the first use of a parallel-plate flow system to apply shear stress to endothelial cells (ECs) and the development of uniaxial substrate stretching techniques (Krueger et al., 1971, "An in Vitro Study of Flow Response by Cells," J. Biomech., 4(1), pp. 31-36 and Meikle et al., 1979, "Rabbit Cranial Sutures in Vitro: A New Experimental Model for Studying the Response of Fibrous Joints to Mechanical Stress," Calcif. Tissue Int., 28(2), pp. 13-144). Since then, a multitude of in vitro devices have been designed and developed for mechanical stimulation of vascular cells and tissues in an effort to better understand their response to in vivo physiologic mechanical conditions. This article reviews the functional attributes of mechanical bioreactors developed in the 21st century, including their major advantages and disadvantages. Each of these systems has been categorized in terms of their primary loading modality: fluid shear stress (FSS), substrate distention, combined distention and fluid shear, or other applied forces. The goal of this article is to provide researchers with a survey of useful methodologies that can be adapted to studies in this area, and to clarify future possibilities for improved research methods.

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Effect of shear stress and substrate on endothelial DAPK expression, caspase activity, and apoptosis

Cited by 26 publications

References 39 publications

An In Vivo Rat Model of Artery Buckling for Studying Wall Remodeling

An In Vivo Rat Model of Artery Buckling for Studying Wall Remodeling

Upregulation of DAPK contributes to homocysteine-induced endothelial apoptosis via the modulation of Bcl2/Bax and activation of caspase 3

Device-Based In Vitro Techniques for Mechanical Stimulation of Vascular Cells: A Review

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