title: Placentomegaly in cloned mouse concepti caused by expansion of the spongiotrophoblast layer.
abstract: Hypertrophic placenta, or placentomegaly, has been reported in cloned cattle and mouse concepti, although their placentation processes are quite different from each other. It is therefore tempting to assume that common mechanisms underlie the impact of somatic cell cloning on development of the trophoblast cell lineage that gives rise to the greater part of fetal placenta. To characterize the nature of placentomegaly in cloned mouse concepti, we histologically examined term cloned mouse placentas and assessed expression of a number of genes. A prominent morphological abnormality commonly found among all cloned mouse placentas examined was expansion of the spongiotrophoblast layer, with an increased number of glycogen cells and enlarged spongiotrophoblast cells. Enlargement of trophoblast giant cells and disorganization of the labyrinth layer were also seen. Despite the morphological abnormalities, in situ hybridization analysis of spatiotemporally regulated placenta-specific genes did not reveal any drastic disturbances. Although repression of some imprinted genes was found in Northern hybridization analysis, it was concluded that this was mostly due to the reduced proportion of the labyrinth layer in the entire placenta, not to impaired transcriptional activity. Interestingly, however, cloned mouse fetuses appeared to be smaller than those of litter size-matched controls, suggesting that cloned mouse fetuses were under a latent negative effect on their growth, probably because the placentas are not fully functional. Thus, a major cause of placentomegaly is expansion of the spongiotrophoblast layer, which consequently disturbs the architecture of the layers in the placenta and partially damages its function.
authors.affiliation: Laboratory of Cellular Biochemistry, Animal Resource Sciences/Veterinary Medical Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Tanaka
authors.forename: M
authors.initials: M
authors.lastname: Oda
authors.forename: Y
authors.initials: Y
authors.lastname: Toyoshima
authors.forename: T
authors.initials: T
authors.lastname: Wakayama
authors.forename: M
authors.initials: M
authors.lastname: Tanaka
authors.forename: N
authors.initials: N
authors.lastname: Yoshida
authors.forename: N
authors.initials: N
authors.lastname: Hattori
authors.forename: J
authors.initials: J
authors.lastname: Ohgane
authors.forename: R
authors.initials: R
authors.lastname: Yanagimachi
authors.forename: K
authors.initials: K
authors.lastname: Shiota
mesh_terms: D000818:Animals; D051792:Basic Helix-Loop-Helix Proteins; D015152:Blotting, Northern; D019976:Cloning, Organism; D004268:DNA-Binding Proteins / Q000235:genetics; D004624:Embryo Transfer; D005260:Female; D020567:Fetal Weight; D015870:Gene Expression; D018392:Genomic Imprinting; D006003:Glycogen / Q000378:metabolism; D006984:Hypertrophy; D017403:In Situ Hybridization; D008098:Litter Size; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D053652:Nuclear Transfer Techniques; D010920:Placenta / Q000378:metabolism / Q000473:pathology*; D010928:Placental Lactogen / Q000235:genetics; D011247:Pregnancy; D014157:Transcription Factors; D014327:Trophoblasts / Q000473:pathology*
chemical_list: D051792:Basic Helix-Loop-Helix Proteins; D004268:DNA-Binding Proteins; D006003:Glycogen; D010928:Placental Lactogen; D014157:Transcription Factors; C489311:Ascl2 protein, mouse