Mahan Sidney, Liu Mingjun, Baylis Richard A, Gomez Delphine
Heart, Lung, Blood and Vascular Medicine Institute, University of Pittsburgh.
Robert M. Berne Cardiovascular Research Center, University of Virginia; Department of Biochemistry and Molecular Genetics, University of Virginia.
J Vis Exp. 2019 Feb 20(144). doi: 10.3791/59139.
Atherosclerosis remains the leading cause of death worldwide and, despite countless preclinical studies describing promising therapeutic targets, novel interventions have remained elusive. This is likely due, in part, to a reliance on preclinical prevention models investigating the effects of genetic manipulations or pharmacological treatments on atherosclerosis development rather than the established disease. Also, results of these studies are often confounding because of the use of superficial lesion analyses and a lack of characterization of lesion cell populations. To help overcome these translational hurdles, we propose an increased reliance on intervention models that employ investigation of changes in cellular composition at a single cell level by immunofluorescent staining and confocal microscopy. To this end, we describe a protocol for testing a putative therapeutic agent in a murine intervention model including a systematic approach for animal dissection, embedding, sectioning, staining, and quantification of brachiocephalic artery lesions. In addition, due to the phenotypic diversity of cells within late-stage atherosclerotic lesions, we describe the importance of using cell-specific, inducible lineage tracing mouse systems and how this can be leveraged for unbiased characterization of atherosclerotic lesion cell populations. Together, these strategies may assist vascular biologists to more accurately model therapeutic interventions and analyze atherosclerotic disease and will hopefully translate into a higher rate of success in clinical trials.
动脉粥样硬化仍然是全球主要的死亡原因,尽管有无数临床前研究描述了有前景的治疗靶点,但新型干预措施仍然难以捉摸。这可能部分归因于依赖临床前预防模型来研究基因操作或药物治疗对动脉粥样硬化发展的影响,而非针对已形成的疾病。此外,由于使用了表面病变分析且缺乏病变细胞群体的特征描述,这些研究结果往往相互矛盾。为了帮助克服这些转化障碍,我们建议更多地依赖干预模型,该模型通过免疫荧光染色和共聚焦显微镜在单细胞水平上研究细胞组成的变化。为此,我们描述了一种在小鼠干预模型中测试假定治疗剂的方案,包括对动物解剖、包埋、切片、染色以及头臂动脉病变定量的系统方法。此外,由于晚期动脉粥样硬化病变内细胞的表型多样性,我们描述了使用细胞特异性、可诱导谱系追踪小鼠系统的重要性,以及如何利用该系统对动脉粥样硬化病变细胞群体进行无偏倚的特征描述。总之,这些策略可能有助于血管生物学家更准确地模拟治疗干预并分析动脉粥样硬化疾病,有望提高临床试验的成功率。