Evidence supporting changes in Nogo-B levels as a marker of neointimal expansion but not adaptive arterial remodeling
Evidence supporting changes in Nogo-B levels as a marker of neointimal expansion but not adaptive arterial remodeling
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DOI：
10.1016/j.vph.2006.11.003
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发表时间：
2007-04-01
影响因子：
4
通讯作者：
Dardik, Alan
中科院分区：
文献类型：
--
作者：
Paszkowiak, Jacek J.;Maloney, Stephen P.;Dardik, Alan
新生内膜增生和向内重塑均可导致再狭窄和管腔丧失。Nogo-B最近被描述为血管损伤和新生内膜增生的抑制剂。为了确定Nogo-B表达是否可能是向内重塑的中介，我们在体内模型中研究了Nogo-B表达的定位，该模型检测了内膜增生和向内重塑。兔颈动脉被球囊损伤，流出支结扎减少流量，或球囊损伤和减少流量。在球囊损伤诱导的新生内膜增生中，Nogo-B在内膜和中膜中的表达减少，而在外膜中的表达则增加。在低流量诱导的内重构中，内侧Nogo-B表达不减少，外膜Nogo-B表达不受刺激。低流量显著增强球囊损伤诱导的新内膜增生，并伴有平滑肌细胞和巨噬细胞中内膜和内侧Nogo-B表达减少，外膜Nogo-B表达增加。低血流诱导的内向重塑与内侧Nogo-B表达的变化无关，与损伤性内膜增生不同。使用正常血流模型抑制内膜增生和再狭窄的药理学策略可能只能部分解释管腔损失，因此可能无法准确预测广泛流出性疾病患者的反应。(c) 2006爱思唯尔公司版权所有。
Both neointimal hyperplasia and inward remodeling contribute to restenosis and lumen loss. Nogo-B has been recently described as an inhibitor of vascular injury and neointimal hyperplasia. To determine whether Nogo-B expression may be a mediator of inward remodeling, we examine the localization of expression of Nogo-B in an in vivo model that examines both neointimal hyperplasia and inward remodeling. The rabbit carotid artery was subjected to balloon injury, outflow branch ligation to reduce flow, or both balloon injury and reduction in flow. In balloon injury-induced neointimal hyperplasia Nogo-B expression was reduced in the intima and media but stimulated in the adventitia. In low flow-induced inward remodeling medial Nogo-B expression was not reduced and adventitial Nogo-B expression was not stimulated. Low flow significantly augmented balloon injury-induced neointimal hyperplasia and was accompanied by reduced intimal and medial Nogo-B expression, and increased adventitial Nogo-B expression in both smooth muscle cells and macrophages. Low flow-induced inward remodeling is not associated with changes in medial Nogo-B expression and is distinct from injury-induced neointimal hyperplasia. Pharmacological strategies to inhibit neointimal hyperplasia and restenosis using normal flow models may only partially account for lumen loss and therefore may not accurately predict responses in patients with extensive outflow disease. (c) 2006 Elsevier Inc. All rights reserved.