A model for studying the effect of shear stress on interactions between vascular endothelial cells and smooth muscle cells

Chiu, Jeng Jiann; Chen, Li Jing; Chen, Cheng Nan; Lee, Pei Ling; Lee, Chih I.

doi:10.1016/j.jbiomech.2003.08.012

Cited by 95 publications

(70 citation statements)

References 23 publications

(25 reference statements)

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“…Lowered wall shear stress has profound effects on endothelial cell phenotype, and it is conceivable that these may in turn influence local VSMCs to modulate and secrete lipoprotein-binding matrix through either direct contact 45,46 or paracrine mediators. 5,47 However, it is also possible that increased circumferential cyclic stretching of the artery wall, which is induced proximal to the constrictive collar and found at natural atherosclerosis-susceptible sites, 2 directly affects phenotypic characteristics of VSMCs. 48 The model of experimentally induced flow changes used in the present study may be a good model system to address these questions.…”

Section: Discussionmentioning

confidence: 99%

Disturbed Laminar Blood Flow Vastly Augments Lipoprotein Retention in the Artery Wall

Steffensen

Mortensen

Kjølby

et al. 2015

ATVB

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Objective— Atherosclerosis develops initially at branch points and in areas of high vessel curvature. Moreover, experiments in hypercholesterolemic mice have shown that the introduction of disturbed flow in straight, atherosclerosis-resistant arterial segments turns them highly atherosclerosis susceptible. Several biomechanical mechanisms have been proposed, but none has been demonstrated. In the present study, we examined whether a causal link exists between disturbed laminar flow and the ability of the arterial wall to retain lipoproteins. Approach and Results— Lipoprotein retention was detected at natural predilection sites of the murine thoracic aorta 18 hours after infusion of fluorescently labeled low-density lipoprotein. To test for causality between blood flow and the ability of these areas to retain lipoproteins, we manipulated blood flow in the straight segment of the common carotid artery using a constrictive collar. Disturbed laminar flow did not affect low-density lipoprotein influx, but increased the ability of the artery wall to bind low-density lipoprotein. Concordantly, disturbed laminar flow led to differential expression of genes associated with phenotypic modulation of vascular smooth muscle cells, increased expression of proteoglycan core proteins associated with lipoprotein retention, and of enzymes responsible for chondroitin sulfate glycosaminoglycan synthesis and sulfation. Conclusions— Blood flow regulates genes associated with vascular smooth muscle cell phenotypic modulation, as well as the expression and post-translational modification of lipoprotein-binding proteoglycan core proteins, and the introduction of disturbed laminar flow vastly augments the ability of a previously resistant, straight arterial segment to retain lipoproteins.

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Section: Discussionmentioning

confidence: 99%

Disturbed Laminar Blood Flow Vastly Augments Lipoprotein Retention in the Artery Wall

Steffensen

Mortensen

Kjølby

et al. 2015

ATVB

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show abstract

“…Atheroprone flow decreases VSMC gene expression (a-SMA and myocardin) and induces a proinflammatory phenotype in ECs and VSMCs by upregulating expression of VCAM-1, IL-8 and monocyte chemoattractant protein-1 (MCP-1) [111]. Shear stress downregulates pathophysiologically relevant gene expression under EC-VSMC co-culture [95,97].…”

mentioning

confidence: 99%

Biomechanical regulation of vascular smooth muscle cell functions: from in vitro to in vivo understanding

Qiu

Zheng

et al. 2014

J. R. Soc. Interface.

147

115

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Vascular smooth muscle cells (VSMCs) have critical functions in vascular diseases. Haemodynamic factors are important regulators of VSMC functions in vascular pathophysiology. VSMCs are physiologically active in the threedimensional matrix and interact with the shear stress sensor of endothelial cells (ECs). The purpose of this review is to illustrate how haemodynamic factors regulate VSMC functions under two-dimensional conditions in vitro or three-dimensional co-culture conditions in vivo. Recent advances show that high shear stress induces VSMC apoptosis through endothelial-released nitric oxide and low shear stress upregulates VSMC proliferation and migration through platelet-derived growth factor released by ECs. This differential regulation emphasizes the need to construct more actual environments for future research on vascular diseases (such as atherosclerosis and hypertension) and cardiovascular tissue engineering.

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“…ese cells work independently and cooperatively to ensure the functional integrity of blood vessels [14]. Traditional methods of co-culture were not suitable to investigate the interaction of these vascular cells.…”

Section: Discussionmentioning

confidence: 99%

IL-8 reduces VCAM-1 secretion of smooth muscle cells by increasing p-ERK expression when 3-D co-cultured with vascular endothelial cells

Zhi

Chu²,

Wu³

et al. 2011

CIM

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Objective: e goal of this study was to investigate the crosstalk between vascular endothelial cells (ECs) and smooth muscle cells (SMCs) using a three-dimensional (3-D) coculture model. In addition, the role of IL-8 in this crosstalk was investigated.Methods: A 3-D co-culture model was constructed using a Transwell chamber system and type I collagen gel. Human umbilical artery smooth muscle cells (HUASMCs) were suspended in the gel and added to the upper compartment of the Transwell. Human umbilical vein endothelial cells (HUVECs) were then grown on the surface of the gel. e growth of HUASMCs was tested with a CFDA SE cell proliferation kit. IL-8 and other bioactive substances were investigated by ELISA and real-time PCR. e alteration of p-ERK expression related to the change in IL-8 levels was also examined by Western blot analysis.Results: e proliferation rate of HUASMCs in the 3-D co-culture model was 0.679 ± 0.057. Secretion and transcription of VEGF, t-PA, NO and VCAM-1 in the 3-D coculture model were di erent than in single (2-D) culture. When 3-D co-cultured, IL-8 released by HUVECs was signi cantly increased (2.35 ± 0.16 fold) (P 0.05) and the expression of VCAM-1 from HUASMCs was reduced accordingly (0.55±0.09 fold). In addition, increasing or decreasing the level of IL-8 changed the level of p-ERK and VCAM-1 expression. e reduction of VCAM-1, resulting from increased IL-8, could be blocked by the MEK inhibitor, PD98059. Conclusion:Crosstalk between HUVECs and HUASMCs occurred and was probably mediated by IL-8 in this 3-D co-culture model.

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A model for studying the effect of shear stress on interactions between vascular endothelial cells and smooth muscle cells

Cited by 95 publications

References 23 publications

Disturbed Laminar Blood Flow Vastly Augments Lipoprotein Retention in the Artery Wall

Disturbed Laminar Blood Flow Vastly Augments Lipoprotein Retention in the Artery Wall

Biomechanical regulation of vascular smooth muscle cell functions: from in vitro to in vivo understanding

IL-8 reduces VCAM-1 secretion of smooth muscle cells by increasing p-ERK expression when 3-D co-cultured with vascular endothelial cells

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