Departament de Patología Mitocondrial i Neuromuscular, Hospital Universitari Vall d'Hebron Institut de Recerca, Universitat Autònoma de Barcelona, Barcelona, Spain.
Neuromuscul Disord. 2013 Apr;23(4):330-6. doi: 10.1016/j.nmd.2013.01.001. Epub 2013 Jan 31.
We report a heteroplasmic novel mutation m.5658T>C in the mt-tRNA(Asn) gene in a patient who initially presented myopathy, bilateral ptosis and ophthalmoparesis and several years later developed a non-nephrotic proteinuria. The muscle biopsy showed cytochrome c oxidase (COX) negative and ragged red fibers and in the kidney biopsy that was taken in order to identify the causes of non-nephrotic proteinuria, a focal segmental glomerulosclerosis was observed. Using laser capture microdissection we isolated COX negative fibers and COX positive fibers from the muscle of the patient and determined that there was a clear increase in the mutation load in the COX negative muscle fibers. However, the low degree of mutation load found in the renal biopsy of the patient does not allow us to conclude that the m.5658T>C mutation is responsible for focal glomerulosclerosis. Additionally, we hypothesize that the mutated m.5658T nucleotide might be structurally relevant, as it is one of the fifteen nucleotides conserved in all the species analyzed and is situated contiguously to the discriminator base in the 3'end of the mt-tRNA, where the tRNase Z cleaves the 3' trailer sequence during mt-tRNA maturation.
我们报告了一位患者的 mt-tRNA(Asn) 基因中存在异质体新型突变 m.5658T>C,该患者最初表现为肌病、双侧上睑下垂和眼肌麻痹,几年后出现非肾病性蛋白尿。肌肉活检显示细胞色素 c 氧化酶 (COX) 阴性和红纤维破碎,在为了确定非肾病性蛋白尿的原因而进行的肾活检中,观察到局灶节段性肾小球硬化。使用激光捕获显微切割,我们从患者的肌肉中分离出 COX 阴性纤维和 COX 阳性纤维,并确定 COX 阴性肌肉纤维中的突变负荷明显增加。然而,患者肾活检中发现的突变负荷程度较低,无法得出 m.5658T>C 突变是导致局灶性肾小球硬化的结论。此外,我们假设突变的 m.5658T 核苷酸可能具有结构相关性,因为它是所有分析物种中保守的十五个核苷酸之一,并且位于 mt-tRNA 3'末端的判别碱基附近,在 mt-tRNA 成熟过程中,tRNase Z 在该位置切割 3'尾部序列。