Intimal Hyperplasia

Davies, Mark G.

doi:10.1016/b978-1-4160-5223-4.00005-6

Cited by 5 publications

(5 citation statements)

References 354 publications

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“…28 Herein, we demonstrate that alcohol treatment inhibits HCASMC proliferation in vitro and that daily feeding of alcohol, in amounts considered equivalent to those found in moderate drinkers, inhibited carotid artery vessel remodeling (ie, intimal-medial thickening) in response to flow reduction. Because SMCs are the predominant cell type responsible for intimal-medial thickening in this model 23,29 and given our in vitro findings, our data are supportive of the concept that moderate alcohol consumption inhibits SMC proliferation and, thus, vascular remodeling. EtOH feeding also strongly inhibited the increase in adventitial volume seen in this model.…”

Section: Discussionsupporting

confidence: 86%

Alcohol Inhibits Smooth Muscle Cell Proliferation via Regulation of the Notch Signaling Pathway

Morrow

Cullen

Liu

et al. 2010

ATVB

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Objective To determine the role of Notch signaling in mediating alcohol’s inhibition of smooth muscle cell (SMC) proliferation. Methods and Results Treatment of human coronary artery SMCs with ethanol (EtOH) decreased Notch 1 mRNA and Notch 1 intracellular domain protein levels, in the absence of any effect on Notch 3. EtOH treatment also decreased C-promoter binding factor-1 (CBF-1)/recombination signal-binding protein (RBP)-jk promoter activity and Notch target gene (hairy related transcription factor [HRT-1] or HRT-2) expression. These effects were concomitant with an inhibitory effect of EtOH on SMC proliferation. Overexpression of constitutively active Notch 1 intracellular domain or human hairy related transcription factor-1 (hHRT-1) prevented the EtOH-induced inhibition of SMC proliferation. In vivo, Notch 1 and HRT-1 mRNA expression was increased after ligation-induced carotid artery remodeling. The vessel remodeling response was inhibited in mice that received “moderate” amounts of alcohol by gavage daily; intimal-medial thickening was markedly reduced, and medial and neointimal SMC proliferating cell nuclear antigen expression was decreased. Moreover, Notch 1 and HRT-1 expression, induced after ligation injury, was inhibited by moderate alcohol consumption. Conclusion EtOH inhibits Notch signaling and, subsequently, SMC proliferation, in vitro and in vivo. The modulation of Notch signaling in SMCs by EtOH may be relevant to the cardiovascular protective effects of moderate alcohol consumption purported by epidemiological studies.

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Section: Discussionsupporting

confidence: 86%

Alcohol Inhibits Smooth Muscle Cell Proliferation via Regulation of the Notch Signaling Pathway

Morrow

Cullen

Liu

et al. 2010

ATVB

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“…As a result, decellularized xenografts have emerged as a new hope for the development of small-caliber vascular grafts (7,8).a or_748 448.. 455 Intimal hyperplasia is characterized by the infiltration of macrophages and the proliferation of smoothmuscle cells in the arterial wall, which, in turn, contribute to the subsequent vascular injury and graft failure after implantation (9,10). As early as 6 h after implantation, macrophages are found to have infiltrated to the graft media (11). These accumulated macrophages can release a number of inflammatory products, including chemotactic factors, oxygen free radicals, and growth factors, contributing to proliferation and migration of smooth-muscle cells (12).…”

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confidence: 99%

Heparin Coating of Small‐Caliber Decellularized Xenografts Reduces Macrophage Infiltration and Intimal Hyperplasia

Cai

Wang

et al. 2009

Artificial Organs

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Small-caliber decellularized xenografts with surface heparin coating are known to reduce in vivo thrombogenicity. This study was performed to examine whether heparin coating on the small-caliber decellularized xenografts would reduce macrophage infiltration and intimal hyperplasia. In a rabbit model of bilateral carotid implantation, each of the animals (n = 18) received a heparin-coated decellularized xenograft from a canine carotid artery on one side and a nonheparin-coated one on the other side. These experiments were terminated respectively at 1 week (n = 6), 3 weeks (n = 6), and 12 weeks (n = 6). Results showed that, compared with the nonheparin-coated grafts, the heparin-coated grafts had significantly less macrophage infiltration 1 week after implantation, identified by the mouse antirabbit macrophage antibody (RAM11)-positive cells on the vascular wall, covering all the proximal, middle, and distal parts of the grafts (P < 0.01). Moreover, the heparin-coated grafts also showed less deposition of proliferation cell nuclear antigen (PCNA)-positive cells on the vascular wall, indicating less cell proliferation, which was significant not only at 1 week (P < 0.01) but also at 12 weeks (P < 0.01). Intimal hyperplasia, measured by the intimal : media (I : M) ratio, was found similar in both groups at 1 and 3 weeks. However, the I : M ratio was significantly lower in the heparin-coated group than in the nonheparin-coated group at 12 weeks, especially in the proximal anastomosis area (0.76 +/- 0.12 vs. 0.345 +/- 0.06, P < 0.01). Heparin coating of small-caliber decellularized xenografts is associated with an early reduction of macrophage infiltration and intimal hyperplasia in a rabbit model of bilateral carotid artery implantation for 12 weeks. Thus, heparin coating appears to deliver not only the antithrombogeneity but also the antiproliferative property for small-caliber decellularized xenografts.

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“…Davies and Hagen 48 have shown that an extensive loss of endothelial cells was observed in the intima at the early stage of vein grafts. It is well established that endothelial cells of vein grafts are derived from circulating progenitor cells, of which one-third are derived from bone marrow progenitor cells.…”

Section: Future Directionsmentioning

confidence: 98%

Gene Therapy for Vein Graft Failure

2013

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The main pathologenesis of vein graft restenosis is neointimal hyperplasia associated with vascular smooth muscle cell migration and proliferation. Gene therapy offers a novel treatment method for reducing or delaying early thrombosis, intimal hyperplasia, and late atherosclerosis. In this review, we will (1) describe sequential pathologies of vein graft disease; (2) summarize the applications of gene therapy in vein graft restenosis; and (3) discuss novel gene therapy for vein graft failure.

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Intimal Hyperplasia

Cited by 5 publications

References 354 publications

Alcohol Inhibits Smooth Muscle Cell Proliferation via Regulation of the Notch Signaling Pathway

Alcohol Inhibits Smooth Muscle Cell Proliferation via Regulation of the Notch Signaling Pathway

Heparin Coating of Small‐Caliber Decellularized Xenografts Reduces Macrophage Infiltration and Intimal Hyperplasia

Gene Therapy for Vein Graft Failure

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