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在一个离体股动脉模型中,由于壁面切应力改变导致的炎性单核细胞反应。

Inflammatory monocyte response due to altered wall shear stress in an isolated femoral artery model.

作者信息

Kadam Aparna A, Gersch Robert P, Rosengart Todd K, Frame Mary D

机构信息

Department of Biomedical Engineering, Physiology and Biophysics, Stony Brook University, Stony Brook, NY 11794-5281, USA.

Department of Surgery, Stony Brook University, Stony Brook, NY 11794-5281, USA.

出版信息

J Biol Methods. 2019 Feb 20;6(1):e109. doi: 10.14440/jbm.2019.274. eCollection 2019.

DOI:10.14440/jbm.2019.274
PMID:31453258
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6706128/
Abstract

Arteriogenesis (collateral formation) is accompanied by a pro-inflammatory state that may be related to the wall shear stress (WSS) within the neo-collateral vessels. Examining the pro-inflammatory component or is complex. In an mouse femoral artery perfusion model, we examined the effect of wall shear stress on pro-arteriogenic inflammatory markers and monocyte adhesion. In a femoral artery model with defined pulsatile flow, WSS was controlled (at physiological stress, 1.4×, and 2× physiological stress) during a 24 h perfusion before gene expression levels and monocyte adhesion were assessed. Significant upregulation of expression was found for the cytokine TNFα, adhesion molecule ICAM-1, growth factor TGFβ, and the transcription factor Egr-1 at varying levels of increased WSS compared to physiological control. Further, trends toward upregulation were found for FGF-2, the cytokine MCP-1 and adhesion molecules VCAM-1 and P-selectin with increased WSS. Finally, monocytes adhesion increased in response to increased WSS. We have developed a murine femoral artery model for studying changes in WSS and show that the artery responds by upregulating inflammatory cytokines, adhesion molecules and growth factors consistent with previous findings.

摘要

动脉生成(侧支形成)伴随着一种促炎状态,这种状态可能与新生侧支血管内的壁面剪应力(WSS)有关。研究促炎成分很复杂。在一个小鼠股动脉灌注模型中,我们研究了壁面剪应力对促动脉生成炎症标志物和单核细胞黏附的影响。在一个具有特定脉动血流的股动脉模型中,在评估基因表达水平和单核细胞黏附之前,在24小时灌注过程中控制壁面剪应力(处于生理应力、1.4倍生理应力和2倍生理应力)。与生理对照相比,在不同程度增加的壁面剪应力下,细胞因子TNFα、黏附分子ICAM-1、生长因子TGFβ和转录因子Egr-1的表达均有显著上调。此外,随着壁面剪应力增加,FGF-2、细胞因子MCP-1以及黏附分子VCAM-1和P-选择素呈现上调趋势。最后,单核细胞黏附随着壁面剪应力增加而增加。我们开发了一种用于研究壁面剪应力变化的小鼠股动脉模型,并表明该动脉通过上调炎症细胞因子、黏附分子和生长因子做出反应,这与先前的研究结果一致。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2617/6706128/969b9c43480b/jbm-6-1-e109-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2617/6706128/525d3c18ef52/jbm-6-1-e109-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2617/6706128/1011257d9cec/jbm-6-1-e109-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2617/6706128/f0c90e0f4f11/jbm-6-1-e109-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2617/6706128/969b9c43480b/jbm-6-1-e109-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2617/6706128/525d3c18ef52/jbm-6-1-e109-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2617/6706128/1011257d9cec/jbm-6-1-e109-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2617/6706128/f0c90e0f4f11/jbm-6-1-e109-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2617/6706128/969b9c43480b/jbm-6-1-e109-g004.jpg

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