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Ooplasm transfer is used to enhance success in human assisted reproduction technologies and can occur during somatic cell nuclear transfer manipulations of embryos of domestic animals. In both cases, the potential exists to create mitochondrial heteroplasmy (the presence of two mitochondrial genotypes within the same cell or individual), because donor cell mitochondria of one genotype are transferred and may persist within the recipient oocyte/embryo. In work reported on p. 569 of this issue, Acton et al. studied heteroplasmic mice and monitored their cardiovascular function, metabolism, hematological parameters, body mass analysis, ovarian reserve, and tissue histology. The heteroplasmic mice displayed hypertension that corrected over time, as well as increased body and fat mass, and abnormalities in electrolytes and hematological parameters. These observations raise new concerns about potential effects of cytoplasm transfer and ooplasm donation on health of offspring in assisted reproduction and indicate potential effects in animals resulting from nuclear transfer procedures.
B. M. Acton, I. Lai, X. Shang, A. Jurisicova, and R. F. Casper. Neutral Mitochondrial Heteroplasmy Alters Physiological Function in Mice. Biol Reprod 2007; 77:569–576. Published online in BOR-Papers in Press 6 June 2007; DOI 10.1095/biolreprod.107.060806
Maternal effects of PTX3 on implantation.
A paper by Tranguch et al. on p. 425 provides insight into mechanisms responsible for reduced litter size in Ptx3-null female mice, previously attributed to fertilization failure. These new results demonstrate transient expression patterns for Ptx3 at the site of implantation, and also that the Il1b gene, encoding a known inducer of Ptx3, is transiently expressed in stromal cells at the implantation site preceding expression of uterine Ptx3 transcript. Together, these observations suggest a role(s) for PTX3 in blastocyst implantation and decidualization. For example, PTX3 binding to the globular domain of complement component C1q might protect the implanting blastocyst from the maternal immune system, and its binding to other molecules, e.g., FGF2, could modulate cell proliferation and angiogenesis during implantation and decidualization. These important new results may be extrapolated to humans, where expression of PTX3 in the uterus during the window of implantation is influenced by a factor(s) from trophoblast cells.
Susanne Tranguch, Anindita Chakrabarty, Yong Guo, Haibin Wang, and Sudhansu K. Dey. Maternal Pentraxin 3 Deficiency Compromises Implantation in Mice. Biol Reprod 2007; 77:425–432. Published online in BOR-Papers in Press 30 May 2007; DOI 10.1095/biolreprod.107.062414
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