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Genetic engineering

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Development of a therapy for compensation of complex I defect

Many mitochondrial diseases are provoked by structural and functional changes in the complex I. Therefore, the major aim of the studies, T. Yagi’s team conducts, is to develop a therapy for compensation of the complex I defect. The most promising method is transfection with NADH gene of yeasts (Saccharomyces cerevisiae). That gene consist of one subunit (Ndi1) responsible for the NADH to ubiquinone-10 (UQ10) electron transfer in the mammalian mitochondria. Using complex I-deficient Chinese hamster CCL16-B2 mutant cell lines, the researchers from T. Yagi’s laboratory performed successful transfection of those cells’ mitochondria with the Ndi1 gene. The Ndi1-transfected cells with functionally active NADH dehydrogenase, as well as the healthy cells (control with the intact complex I gene) showed electron transfer when malate plus glutamate were employed as respiratory substrates. So, thansfection with Ndi1 gene opens new possibilities in the treatment of mitochondrial diseases with the use of gene therapy.