Synergistic Regulation of Angiogenic Sprouting by Biochemical Factors and Wall Shear Stress

Kaunas, Roland; Kang, Hyojeung; Bayless, Kayla J.

doi:10.1007/s12195-011-0208-5

Cited by 42 publications

(44 citation statements)

References 116 publications

(147 reference statements)

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“…Although in vitro models have contributed tremendously to examining the relationship between different cells involved in angiogenesis 3 , their findings and physiological relevance can be undermined due to their limited complexity and the fact that they do not closely reflect an in vivo scenario. To overcome these limitations, three-dimensional culture systems 3 , ex vivo tissue models 4 , microfluidic systems 5,6 , and computational models 7 have been developed and introduced in recent years. However, there is still a need for a model with time-lapse capability to investigate angiogenesis in intact microvascular networks ex vivo .…”

Section: Introductionmentioning

confidence: 99%

An <em>Ex Vivo</em> Method for Time-Lapse Imaging of Cultured Rat Mesenteric Microvascular Networks

Azimi¹,

Motherwell²,

Murfee³

2017

JoVE

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Angiogenesis, defined as the growth of new blood vessels from pre-existing vessels, involves endothelial cells, pericytes, smooth muscle cells, immune cells, and the coordination with lymphatic vessels and nerves. The multi-cell, multi-system interactions necessitate the investigation of angiogenesis in a physiologically relevant environment. Thus, while the use of in vitro cell-culture models have provided mechanistic insights, a common critique is that they do not recapitulate the complexity associated within a microvascular network. The objective of this protocol is to demonstrate the ability to make time-lapse comparisons of intact microvascular networks before and after angiogenesis stimulation in cultured rat mesentery tissues. Cultured tissues contain microvascular networks that maintain their hierarchy. Immunohistochemical labeling confirms the presence of endothelial cells, smooth muscle cells, pericytes, blood vessels and lymphatic vessels. In addition, labeling tissues with BSI-lectin enables time-lapse comparison of local network regions before and after serum or growth factor stimulation characterized by increased capillary sprouting and vessel density. In comparison to common cell culture models, this method provides a tool for endothelial cell lineage studies and tissue specific angiogenic drug evaluation in physiologically relevant microvascular networks.

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Section: Introductionmentioning

confidence: 99%

An <em>Ex Vivo</em> Method for Time-Lapse Imaging of Cultured Rat Mesenteric Microvascular Networks

Azimi¹,

Motherwell²,

Murfee³

2017

JoVE

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“…During angiogenesis, endothelial cells (ECs) respond to biochemical factors such as vascular endothelial growth factor (VEGF) [2], basic fibroblast growth factor (bFGF) [3], placental growth factor [4], and sphingosine 1-phosphate (S1P) [5], as well as mechanical shear forces created by blood flow [6]. Wall shear stress (WSS) rates have been estimated at 1–8 dyn/cm 2 for the microcirculation, the site of angiogenic initiation [7].…”

Section: Introductionmentioning

confidence: 99%

Fluid shear stress promotes proprotein convertase-dependent activation of MT1-MMP

Kang

Duran

Abbey

et al. 2015

Biochemical and Biophysical Research Communications

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During angiogenesis, endothelial cells (ECs1) initiate new blood vessel growth and invade into the extracellular matrix (ECM). Membrane type-1 matrix metalloproteinase (MT1-MMP) facilitates this process and translocates to the plasma membrane following activation to promote ECM cleavage. The N-terminal pro-domain within MT1-MMP must be processed for complete activity of the proteinase. This study investigated whether MT1-MMP activation was altered by sphingosine 1-phosphate (S1P) and wall shear stress (WSS), which combine to stimulate EC invasion in three dimensional (3D) collagen matrices. MT1-MMP was activated rapidly and completely by WSS but not S1P. Proprotein convertases (PCs) promoted MT1-MMP processing, prompting us to test whether WSS or S1P treatments increased PC activity. Like MT1-MMP, PC activity increased with WSS, while S1P had no effect. A pharmacological PC inhibitor completely blocked S1P- and WSS-induced EC invasion and MT1-MMP translocation to the plasma membrane. Further, a recombinant PC inhibitor reduced MT1-MMP activation and decreased lumen formation in invading ECs, a process known to be controlled by MT1-MMP. Thus, we conclude that PC and MT1-MMP activation are mechanosensitive events that are required for EC invasion into 3D collagen matrices.

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“…Increased and asymmetric aortic wall shear stress is the most prevalent flow anomaly in BAV patients with dilated ascending aorta [7,8]. The abnormal force parallel to the aortic wall exerted by shear stress acts upon endothelial surface in terms of friction, which may activate cellular signaling cascades and result in over-expression of extracellular matrix degenerating substances including matrix metalloproteinases (MMPs) and their endogenous tissue inhibitors (TIMPs) [9,10].…”

Section: Introductionmentioning

confidence: 99%

Circulating matrix metalloproteinase patterns in association with aortic dilatation in bicuspid aortic valve patients with isolated severe aortic stenosis

Wang

Dong

et al. 2014

Heart Vessels

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Bicuspid aortic valve (BAV) exhibits a clinical incline toward aortopathy, in which aberrant tensile and shear stress generated by BAV can induce differential expression of matrix metalloproteinases (MMPs) and their endogenous tissue inhibitors (TIMPs). Whether stenotic BAV, which exhibits additional eccentric high-velocity flow jet upon ascending aorta and further worsens circumferential systolic wall shear stress than BAV with echocardiographically normal aortic valve, can lead to unique plasma MMP/TIMP patterns is still unknown. According to their valvulopathy and aortic dilatation status, 93 BAV patients were included in the present study. Group A (n = 37) and B (n = 28) comprised severely stenotic patients with or without ascending aorta dilatation; Group C (n = 12) and D (n = 16) comprised echocardiographically normal BAV patients with or without ascending aorta dilatation. Plasma MMP/TIMP levels (MMP-1, -2, -3, -8, -9, -10, -13 and TIMP-1, -2, -4) were determined via a multiplex ELISA detection system in a single procedure. Among patients with isolated severe aortic stenosis, plasma levels of MMP-2 and -9 were significantly elevated when ascending aortic dilatation was present (p = 0.001 and p = 0.002, respectively). MMP-2, however, remained as the single elevated plasma component among echocardiographically normal BAV patients with dilated ascending aorta (p = 0.027). Multivariate analysis revealed that MMP-2 and MMP-9 could both serve as independent risk factor for aortic dilatation in the case of isolated severe stenosis (p = 0.003 and p = 0.001, respectively), and MMP-2 in echocardiographically normal patients (p = 0.002). In conclusion, BAV patients with isolated severe aortic stenosis demonstrated a distinct plasma MMP/TIMP pattern, which might be utilized as circulating biomarkers for early detection of aortic dilatation.

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Synergistic Regulation of Angiogenic Sprouting by Biochemical Factors and Wall Shear Stress

Cited by 42 publications

References 116 publications

An <em>Ex Vivo</em> Method for Time-Lapse Imaging of Cultured Rat Mesenteric Microvascular Networks

An <em>Ex Vivo</em> Method for Time-Lapse Imaging of Cultured Rat Mesenteric Microvascular Networks

Fluid shear stress promotes proprotein convertase-dependent activation of MT1-MMP

Circulating matrix metalloproteinase patterns in association with aortic dilatation in bicuspid aortic valve patients with isolated severe aortic stenosis

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