Department of Gene Therapy, Jikei University School of Medicine, Tokyo 105-8461, Japan.
Proc Natl Acad Sci U S A. 2010 Apr 27;107(17):7886-91. doi: 10.1073/pnas.1002758107. Epub 2010 Apr 12.
Most lysosomal storage diseases (LSDs) are life-threatening genetic diseases. The pathogenesis of these diseases is poorly understood. Induced pluripotent stem (iPS) cell technology offers new opportunities for both mechanistic studies and development of stem cell- based therapies. Here we report the generation of disease-specific iPS cells from mouse models of Fabry disease, globoid cell leukodystrophy (GLD), and mucopolysaccharidosis VII (MPSVII). These mouse model-derived iPS cells showed defects in disease-specific enzyme activities and significant accumulation of substrates for these enzymes. In the lineage-directed differentiation studies, Fabry-iPS and GLD-iPS cells were efficiently differentiated into disease-relevant cell types, such as cardiomyocytes and neural stem cells, which might be useful in mechanistic and therapeutic studies. Notably, MPSVII-iPS cells demonstrated a markedly impaired ability to form embryoid bodies (EBs) in vitro. MPSVII-EBs exibited elevated levels of hyaluronan and its receptor CD44, and markedly reduced expression levels of E-cadherin and cell-proliferating marker. Partial correction of enzyme deficiency in MSPVII-iPS cells led to improved EB formation and reversal of aberrant protein expression. These data indicate a potential mechanism for the partial lethality of MPSVII mice in utero, and suggest a possible abnormality of embryonic development in MPSVII patients. Thus, our study demonstrates the unique promise of iPS cells for studying the pathogenesis and treatment of LSDs.
大多数溶酶体贮积症(LSD)是危及生命的遗传疾病。这些疾病的发病机制尚不清楚。诱导多能干细胞(iPS)细胞技术为机制研究和基于干细胞的治疗方法的发展提供了新的机会。在这里,我们报告了从小鼠模型的法布里病、球形细胞脑白质营养不良(GLD)和黏多糖贮积症 VII 型(MPSVII)中生成疾病特异性 iPS 细胞。这些来自小鼠模型的 iPS 细胞显示出疾病特异性酶活性的缺陷和这些酶的底物的显著积累。在谱系定向分化研究中,法布里 iPS 和 GLD-iPS 细胞有效地分化为与疾病相关的细胞类型,如心肌细胞和神经干细胞,这可能有助于机制和治疗研究。值得注意的是,MPSVII-iPS 细胞在体外形成类胚体(EBs)的能力明显受损。MPSVII-EBs 表现出透明质酸及其受体 CD44 的水平升高,以及 E-钙粘蛋白和细胞增殖标志物的表达水平明显降低。MPSVII-iPS 细胞中酶缺陷的部分纠正导致 EB 形成的改善和异常蛋白表达的逆转。这些数据表明了 MPSVII 小鼠在子宫内部分致死的潜在机制,并提示了 MPSVII 患者胚胎发育的可能异常。因此,我们的研究表明 iPS 细胞在研究 LSD 发病机制和治疗方法方面具有独特的潜力。