Wang Hui, Pan Yunzhu, Zhang Zaiqiang, Li Xingang, Xu Zhe, Suo Yue, Li Wei, Wang Yongjun
Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
China National Clinical Research Center for Neurological Diseases, Beijing, China.
J Mol Neurosci. 2017 Feb;61(2):221-226. doi: 10.1007/s12031-017-0881-5. Epub 2017 Feb 3.
Familial cerebral cavernous malformation (FCCM) is a vascular malformation disorder that closely associated with three identified genes: KRIT1/CCM1, MGC4607/CCM2, and PDCD10/CCM3. Here, we present a Chinese family affected by FCCM due to a novel KRIT1/CCM1 insertion mutation. The proband was hospitalized for sudden unconsciousness and underwent surgical treatment. The section of lesions showed classical cavernous-dilated vessels without intervening brain parenchyma, and hemosiderin-laden macrophages were accumulated in the surrounding tissue. In addition, magnetic resonance imaging (MRI) showed severe multiple cerebral cavernous malformation (CCM) lesions in cerebrum, brainstem, and cerebellum in other affected subjects. Especially, for the proband's mother, hundreds of lesions were presented, and a few lesions were found in the expanded lateral ventricle (Evans' index =0.33). Moreover, she showed the similar symptoms of hydrocephalus, including headache, dizziness, and diplopia. It was extremely rare in previous reports. To date, the genetic alterations leading to FCCM in Chinese population remain largely unknown. We investigated genetic defects of this family. Sequence analyses disclosed a novel heterozygous insertion mutation (c.1896_1897insT; p.Pro633SerfsTer22) in KRIT1/CCM1. Moreover, our real-time PCR results revealed that the mRNA level of KRIT1/CCM1 were significantly decreased in FCCM subjects (CCM family =0.42 ± 0.20 vs. healthy control =1.01 ± 0.16, P = 0.004). It indicated that this mutation could cause KRIT1/CCM1 functional mRNA deficiency. It may be closely related with the pathogenesis of FCCM. Our findings provided a new gene mutation profile which will be of great significance in early diagnosis and appropriate clinical surveillance of FCCM patients.
家族性脑海绵状血管畸形(FCCM)是一种血管畸形疾病,与三个已确定的基因密切相关:KRIT1/CCM1、MGC4607/CCM2和PDCD10/CCM3。在此,我们报告一个因新型KRIT1/CCM1插入突变而患FCCM的中国家系。先证者因突发意识丧失入院并接受手术治疗。病变切片显示典型的海绵状扩张血管,其间无脑实质,周围组织中有含铁血黄素沉积的巨噬细胞积聚。此外,磁共振成像(MRI)显示其他受影响个体的大脑、脑干和小脑存在严重的多发性脑海绵状血管畸形(CCM)病变。特别是先证者的母亲,有数百个病变,在扩大的侧脑室中发现了一些病变(埃文斯指数=0.33)。此外,她表现出类似脑积水的症状,包括头痛、头晕和复视。这在以前的报告中极为罕见。迄今为止,导致中国人群FCCM的基因改变在很大程度上仍不清楚。我们对这个家系进行了基因缺陷研究。序列分析揭示了KRIT1/CCM1中一个新的杂合插入突变(c.1896_1897insT;p.Pro633SerfsTer22)。此外,我们的实时PCR结果显示,FCCM患者中KRIT1/CCM1的mRNA水平显著降低(CCM家系=0.42±0.20,健康对照=1.01±0.16,P=0.004)。这表明该突变可能导致KRIT1/CCM1功能性mRNA缺乏。它可能与FCCM的发病机制密切相关。我们的发现提供了一个新的基因突变谱,这对FCCM患者的早期诊断和适当的临床监测具有重要意义。