Department of Pediatrics, Division of Genetics and Metabolism, University of California, Irvine, California, USA.
Clin Transl Sci. 2012 Jun;5(3):226-34. doi: 10.1111/j.1752-8062.2012.00407.x. Epub 2012 Apr 4.
Inclusion body myopathy associated with Paget's disease of bone and frontotemporal dementia (IBMPFD) is an autosomal dominant disorder caused by mutations in the Valosin-containing protein (VCP) gene on chromosome 9p12-13. Patients demonstrate limb girdle muscle weakness, which eventually progresses to involve respiratory muscles, and death from respiratory and cardiac failure. This is the first investigation to analyze key molecular mediators and signaling cascades in skeletal muscle causing myopathy by global gene microarray in hopes of understanding the dysregulated genes and molecular mechanisms underlying IBMPFD and the hope of finding novel therapeutic targets. We determined expression profiles using Human Genome Array microarray technology in Vastus lateralis muscles from patients and their first-degree relatives. We analyzed gene annotations by Database for Annotation, Visualization and Integration Discovery and identified differentially dysregulated genes with roles in several novel biological pathways, including regulation of actin cytoskeleton, ErbB signaling, cancer, in addition to regulation of autophagy, and lysosomal signaling, known disrupted pathways in VCP disease. In this report, we present data from the first global microarray analyzing IBMPFD patient muscles and elucidating dysregulated pathways to further understand the pathogenesis of the disease and discover potential therapeutics.
伴有骨 Paget 病和额颞叶痴呆的包涵体肌病(IBMPFD)是一种常染色体显性疾病,由 9p12-13 染色体上的含缬氨酸蛋白(VCP)基因突变引起。患者表现为肢体带肌无力,最终进展为呼吸肌受累,并因呼吸和心力衰竭而死亡。这是首次通过全球基因微阵列分析来研究导致肌病的骨骼肌肉中的关键分子介质和信号级联,以期了解 IBMPFD 背后失调的基因和分子机制,并希望找到新的治疗靶点。我们使用人类基因组阵列微阵列技术在患者及其一级亲属的股外侧肌中确定了表达谱。我们通过数据库进行基因注释分析,用于注释、可视化和综合发现,并确定了具有几种新生物学途径作用的差异失调基因,包括肌动蛋白细胞骨架调节、ErbB 信号、癌症,除了自噬和溶酶体信号调节,这些都是 VCP 疾病中失调的途径。在本报告中,我们提供了首次对 IBMPFD 患者肌肉进行全球微阵列分析的数据,并阐明了失调的途径,以进一步了解疾病的发病机制并发现潜在的治疗方法。