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Developmental arrest of scNT‐derived fetuses by disruption of the developing endometrial gland as a result of impaired trophoblast migration and invasiveness
Author(s) -
Kim JaeHwan,
Park JongYi,
Park MiRung,
Hwang KyuChan,
Park KeunKyu,
Park Chankyu,
Cho SeongKeun,
Lee HwiCheul,
Song Hyuk,
Park SooBong,
Kim Teoan,
Kim JinHoi
Publication year - 2011
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22568
Subject(s) - somatic cell nuclear transfer , cytotrophoblast , biology , trophoblast , placenta , andrology , embryo , fetus , embryogenesis , microbiology and biotechnology , blastocyst , pregnancy , genetics , medicine
Somatic cell nuclear transfer (scNT)‐derived pig placenta tissues of gestational day 30 displayed avascularization and hypovascularization. Most of the cytotrophoblast‐like cells of the developing scNT‐derived placenta villi were improperly localized or exhibited impaired migration to their targeting loci. Id‐2, Met, MMP‐9, and MCM‐7 were barely detectable in the cytotrophoblast cells of the scNT‐derived placenta villi. Active MMP‐2 and MMP‐9 expression was significantly down‐regulated in the scNT‐embryo transferred recipient uteri. scNT clones exhibited a hypermethylated pattern within the pig MMP‐9 promoter region and the significance of GC box in the regulation of MMP‐9 promoter activity. Marked apoptosis was observed in the developing endometrial gland of scNT‐embryo transferred recipient uteri. Collectively, our data strongly indicated that early gestational death of scNT clones is caused, at least in part, by disruption of the developing endometrial gland as a result of impaired trophoblast migration and invasiveness due to the down‐regulation of active MMP‐9 expression. Developmental Dynamics 240:627–639, 2011. © 2011 Wiley‐Liss, Inc.