Graft-Extrinsic Cells Predominate in Vein Graft Arterialization

Zhang, Lisheng; Freedman, Neil J.; Brian, Leigh; Peppel, Karsten

doi:10.1161/01.atv.0000116865.98067.31

Cited by 71 publications

(65 citation statements)

References 44 publications

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“…After vein grafting in this murine model, most of the cells die and are repopulated by recipient cells from the circulation and surrounding tissues. 23,56 Therefore, this murine model is not same as human vein grafts; however, in the present study, we used this model to address the important role of IL-1/IL-18, inflammation, and neointima formation, which are the main events of human venous bypass graft remodeling.…”

Section: Discussionmentioning

confidence: 99%

Cross Talk Between Vascular Smooth Muscle Cells and Monocytes Through Interleukin-1β/Interleukin-18 Signaling Promotes Vein Graft Thickening

et al. 2014

ATVB

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Objective-Interleukin (IL)-1β and IL-18 are key proinflammatory cytokines that play important roles in the pathophysiology of vein graft remodeling. However, the mechanism of IL-1β/IL-18 production and its role in the development of graft remodeling remain unclear. Approach and Results-IL-1β/IL-18 were rapidly expressed in venous interposition grafts. Vascular smooth muscle cell (VSMC) death and monocytic inflammasome activation occurred in grafted veins. Necrotic VSMCs induced the expression of IL-1β, IL-18, and other inflammasome-associated proteins in monocytes, which was partially inhibited by their antagonist, recombinant IL-1ra-Fc-IL-18bp. Activated monocytes stimulated proliferation of VSMCs by activating cell growth-related signaling molecules (AKT, STAT3, ERK1/2, and mTOR [AKT/protein kinase B, signal transducer and activator of transcription 3, extracellular signal-regulated kinase 1/2, mammalian target of rapamycin]) and increasing production of platelet-derived growth factor-bb; these effects were suppressed by IL-1ra-Fc-IL-18bp. Activated monocytes also promoted migration of VSMCs, which was independent of IL-1β/IL-18 signaling. Importantly, administration of IL-1ra-Fc-IL-18bp inhibited activation of cell growth-related signaling molecules, VSMC proliferation, and vein graft thickening in vivo. Conclusions-Our work identified an interaction among necrotic VSMCs, monocytes, and viable VSMCs through IL-1β/ IL-18 signaling, which might be exploited as a therapeutic target in vein graft remodeling. (Arterioscler Thromb Vasc

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Section: Discussionmentioning

confidence: 99%

Cross Talk Between Vascular Smooth Muscle Cells and Monocytes Through Interleukin-1β/Interleukin-18 Signaling Promotes Vein Graft Thickening

et al. 2014

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“…This result suggests that a decline in progenitor cell adhesion, incorporation into the endothelium, and function with age may influence the onset and progression of atherosclerosis. Furthermore, endogenous bone marrow-derived circulating EPCs adhere to sites of acute endothelial injury, such as vein grafts (51,52).…”

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confidence: 99%

Effect of cellular senescence on the albumin permeability of blood-derived endothelial cells

Cheung

Ganatra

Peters

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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Cheung TM, Ganatra MP, Peters EB, Truskey GA. Effect of cellular senescence on the albumin permeability of blood-derived endothelial cells. Am J Physiol Heart Circ Physiol 303: H1374-H1383, 2012. First published September 28, 2012 doi:10.1152/ajpheart.00182.2012In this study, we tested the hypotheses that endothelial cells (ECs) derived from human umbilical cord blood (hCB-ECs) exhibit low permeability, which increases as hCB-ECs age and undergo senescence, and that the change in the permeability of hCB-ECs is due to changes in tight junction protein localization and the activity of exchange protein activated by cAMP (Epac)1. Albumin permeability across lowpassage hCB-EC monolayers on Transwell membranes was 10 times lower than for human aortic ECs (HAECs) (P Ͻ 0.01) but similar to in vivo values in arteries. Expression of the tight junction protein occludin and tyrosine phosphorylation of occludin were less in hCBECs than in HAECs (P Ͻ 0.05). More hCB-ECs than HAECs underwent mitosis (P Ͻ 0.01). hCB-ECs that underwent Ͼ44 population doublings since isolation had a significantly higher permeability than hCB-ECs that underwent Ͻ31 population doublings (P Ͻ 0.05). This age-related increase in hCB-EC permeability was associated with an increase in tyrosine phosphorylation of occludin (P Ͻ 0.01); permeability and occludin phosphorylation were reduced by treatment with 2 M resveratrol. Tyrosine phosphorylation of occludin and cell age influence the permeability of hCB-ECs, whereas levels of EC proliferation and expression of tight junction proteins did not explain the differences between hCB-EC and HAEC permeability. The elevated permeability in late passage hCB-ECs was reduced by 25-40% by elevation of membrane-associated cAMP and activation of the Epac1 pathway. Given the similarity to in vivo permeability to albumin and the high proliferation potential, hCB-ECs may be a suitable in vitro model to study transport-related pathologies and cell aging. vascular biology; cell aging; occludin; endothelial progenitor cell; permeability

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“…Intima and media hyperplasia proliferation manifests cells from diverse origins, including peri-adventitial fibroblasts, bone marrowderived progenitor cells, and smooth muscle cells. As many as 60% of the neo-intima comprises cells originating from outside the adventitia of the graft [19][20][21]. External support targets some of the key factors associated with the development of intimal hyperplasia such as high circumferential wall stress and disturbed flow patterns due to luminal irregularities.…”

Section: Resultsmentioning

confidence: 99%

Inhibition of vein graft remodeling and neo-intimal formation using a cobalt chrome external support

Nitecki¹,

Yosef²,

Tozzi³

et al. 2018

Arch Clin Exp Surg

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IntroductionThe autologous vein bypass remains the most effective and durable revascularization strategy for patients with critical limb ischemia [1]. However, despite significant advances in the understanding of venous pathophysiology post-implantation, little progress was made in the clinical setting in which vein graft failure rate is still 30 -50% within 3 to 5 years [1,2].Early graft occlusion, within one month from implantation, is generally ascribed to technical or procedural related complications (e.g., kinking and twisting) or poor conduit quality. Late vein graft failure is attributed to the structural changes that occur in the conduit immediately post-implantation due to the exposure to Following completion of the first anastomosis, randomization was performed to allocate the experimental and control grafts in each animal. Post-procedure, Doppler US was used to assess grafts lumen diameter at T0 and then 3-5 and 12-14 weeks after surgery. At 12-14 weeks, all sheep underwent angiography to assess grafts patency and lumen uniformity (coefficient of variance -CV) after which they were sacrificed, and all grafts were harvested for microscopic histological analysis. Results: Baseline (T0) internal diameter was not significantly different between the supported and unsupported grafts. At twelve to fourteen weeks, the internal diameter of supported grafts remained unchanged and was significantly lower compared to the non-supported grafts (6.6mm±0.4mm vs. 12.8mm±4.0mm respectively, p= 0.0001). Percentage coefficient of variance (%CV) was 4.6% ± 4.3 in the supported grafts as opposed to average CV% of 14.7% ±6.5 in the non-stented group (p=0.011). Neointimal area was significantly lower in the stented compared to the non-stented group (1.4 mm2± 3.3mm2 versus 9.6mm2 ± 9.7mm2 respectively, p=0.009). Inhibition of vein graft remodeling and neo-intimal formation using a cobalt chrome external support Conclusions:External support of vein grafts using a braided cobalt chrome external stent reduces early vein graft remodeling and mitigates the development of neointimal hyperplasia.

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Graft-Extrinsic Cells Predominate in Vein Graft Arterialization

Cited by 71 publications

References 44 publications

Cross Talk Between Vascular Smooth Muscle Cells and Monocytes Through Interleukin-1β/Interleukin-18 Signaling Promotes Vein Graft Thickening

Cross Talk Between Vascular Smooth Muscle Cells and Monocytes Through Interleukin-1β/Interleukin-18 Signaling Promotes Vein Graft Thickening

Effect of cellular senescence on the albumin permeability of blood-derived endothelial cells

Inhibition of vein graft remodeling and neo-intimal formation using a cobalt chrome external support

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