Choi Jaesung P, Yang Xi, Foley Matthew, Wang Xian, Zheng Xiangjian
Lab of Cardiovascular Signaling, Centenary Institute; Faculty of Medicine, Sydney Medical School, University of Sydney.
Department of Pharmacology, School of Basic Medical Sciences, Tianjin Medical University.
J Vis Exp. 2017 Sep 4(127):56476. doi: 10.3791/56476.
Mutations in the CCM1 (aka KRIT1), CCM2, or CCM3 (aka PDCD10) gene cause cerebral cavernous malformation (CCM) in humans. Mouse models of CCM disease have been established by tamoxifen induced deletion of Ccm genes in postnatal animals. These mouse models provide invaluable tools to investigate molecular mechanism and therapeutic approaches for CCM disease. An accurate and quantitative method to assess lesion burden and progression is essential to harness the full value of these animal models. Here, we demonstrate the induction of CCM disease in a mouse model and the use of the contrast enhanced X-ray micro computed tomography (micro-CT) method to measure CCM lesion burden in mouse brains. At postnatal day 1 (P1), we used 4-hydroxytamoxifen (4HT) to activate Cre recombinase activity from the Cdh5-CreErt2 transgene to cleave the floxed allele of Ccm2. CCM lesions in mouse brains were analyzed at P8. For micro-CT, iodine based Lugol's solution was used to enhance contrast in brain tissue. We have optimized the scan parameters and utilized a voxel dimension of 9.5 µm, which lead to a minimum feature size of approximately 25 µm. This resolution is sufficient to measure CCM lesion volume and number globally and accurately, and provide high-quality 3-D mapping of CCM lesions in mouse brains. This method enhances the value of the established mouse models to study the molecular basis and potential therapies for CCM and other cerebrovascular diseases.
CCM1(又称KRIT1)、CCM2或CCM3(又称PDCD10)基因的突变会导致人类脑海绵状畸形(CCM)。通过他莫昔芬诱导出生后动物体内Ccm基因缺失,已建立了CCM疾病的小鼠模型。这些小鼠模型为研究CCM疾病的分子机制和治疗方法提供了宝贵的工具。一种准确且定量的评估病变负担和进展的方法对于充分利用这些动物模型的价值至关重要。在此,我们展示了在小鼠模型中诱导CCM疾病,并使用对比增强X射线微型计算机断层扫描(微型CT)方法来测量小鼠大脑中的CCM病变负担。在出生后第1天(P1),我们使用4-羟基他莫昔芬(4HT)激活来自Cdh5-CreErt2转基因的Cre重组酶活性,以切割Ccm2的floxed等位基因。在P8时分析小鼠大脑中的CCM病变。对于微型CT,使用基于碘的卢戈氏溶液来增强脑组织中的对比度。我们优化了扫描参数,并使用了9.5 µm的体素尺寸,这导致最小特征尺寸约为25 µm。这种分辨率足以全局且准确地测量CCM病变体积和数量,并提供小鼠大脑中CCM病变的高质量三维图谱。这种方法提高了已建立的小鼠模型在研究CCM和其他脑血管疾病的分子基础及潜在治疗方法方面的价值。