Xenogenic transfer of isolated murine mitochondria into human ρ0 cells can improve respiratory function

被引:89
作者
Katrangi, Eyad [1 ]
D'Souza, Gerard [1 ]
Boddapati, Sarathi V. [1 ]
Kulawiec, Mariola [2 ]
Singh, Keshav K. [2 ]
Bigger, Brian [3 ]
Weissig, Volkmar [1 ]
机构
[1] Northeastern Univ, Dept Pharmaceut Sci, Bouve Coll Hlth Sci, Sch Pharm, Boston, MA 02115 USA
[2] Roswell Pk Canc Inst, Dept Canc Genet, Buffalo, NY 14263 USA
[3] Univ Manchester, Royal Manchester Childrens Hosp, Manchester, Lancs, England
关键词
D O I
10.1089/rej.2007.0575
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Mitochondrial DNA mutations are the direct cause of several physiological disorders and are also associated with the aging process. The modest progress made over the past two decades towards manipulating the mitochondrial genome and understanding its function within living mammalian cells means that cures for mitochondrial DNA mutations are still elusive. Here, we report that transformed mammalian cells internalize exogenous isolated mitochondria upon simple co-incubation. We first demonstrate the physical presence of internalized mitochondria within recipient cells using fluorescence microscopy. Second, we show that xenogenic transfer of murine mitochondria into human cells lacking functional mitochondria can functionally restore respiration in cells lacking mtDNA. Third, utilizing the natural competence of isolated mitochondria to take up linear DNA molecules, we demonstrate the feasibility of using cellular internalization of isolated exogenous mitochondria as a potential tool for studying mitochondrial genetics in living mammalian cells.
引用
收藏
页码:561 / 570
页数:10
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