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Yabuuchi A.,Advanced Medical Research Institute of Fertility | Rehman H.,Cornell University | Kim K.,Cornell University
Journal of Mammalian Ova Research | Year: 2012

Parthenogenesis is the process in which an oocyte develops into an embryo without fertilization. Parthenogenetic activation can be performed at various stages of meiosis, yielding embryos with distinct genetic patterns of homozygosity and heterozygosity. Parthenogenetic embryonic stem (pES) cells derived from such embryos have heterozygous patterns that can be identified using genome-wide single nucleotide polymorphism (SNP) analysis, to determine whether extrusion of the first or second polar body has been inhibited. Heterozygous pES cells carrying the full complement of major histocompatibility complex (MHC) antigens matched to the oocyte donor may provide a potential source of immunematched cells and tissues for cell replacement therapy. In this review, we summarize the process of deriving heterozygous MHC-matched pES cells using mouse and human models. © 2012 Japanese Society of Mammalian Ova Research.

Yabuuchi A.,Advanced Medical Research Institute of Fertility | Beyhan Z.,Sher Institute for Reproductive Medicine Las Vegas | Kagawa N.,Advanced Medical Research Institute of Fertility | Mori C.,Advanced Medical Research Institute of Fertility | And 5 more authors.
Biochimica et Biophysica Acta - General Subjects | Year: 2012

Background: Mitochondrial diseases are caused by the mutations in both nuclear and mitochondrial DNA (mtDNA) and the treatment options for patients who have mitochondrial disease are rather limited. Mitochondrial DNA is transmitted maternally and does not follow a Mendelian pattern of inheritance. Since reliable and predictable detection of mitochondrial disorders in embryos and oocytes is unattainable at present, an alternative approach to this problem has emerged as partial or complete replacement of mutated mtDNA with the wild-type mtDNA through embryo manipulations. Currently available methods to achieve this goal are germinal vesicle transfer (GVT), metaphase chromosome transfer (CT), pronuclear transfer (PNT) and ooplasmic transfer (OT). Scope of review: We summarize the state of the art regarding these technologies and discuss the implications of recent advances in the field for clinical practice. Major conclusions: CT, PNT and GVT techniques hold promise to prevent transmission of mutant mtDNA through ARTs. However, it is clear that mtDNA heteroplasmy in oocytes, embryos and offspring produced by these methods remains as a legitimate concern. General significance: New approaches to eliminate transmission of mutant mtDNA certainly need to be explored in order to bring the promise of clinical application for the treatment of mitochondrial disorders. This article is part of a Special Issue entitled Biochemistry of Mitochondria, Life and Intervention 2010. © 2011 Elsevier B.V.

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