Placental Dysfunction in Cloned Pigs Linked to Impaired Trophoblast Adhesion and Vascular Development

Animal cloning, while promising for livestock breeding and genetic improvement, is hampered by low efficiency largely due to placental abnormalities. This study investigated this issue in cloned pigs at the 35th day of gestation, where a 69.8% developmental abnormality rate was observed. Morphological analyses revealed structural defects in placentas from failed pregnancies, including delayed fold development and abnormal areolae formation, coupled with reduced endometrial glands and maternal-side blood vessels. Immunohistochemistry demonstrated impaired placental function, evidenced by aberrant E-cadherin expression compromising trophoblast adhesion, and significantly reduced glycogen/polysaccharide secretion. Furthermore, Plet1 expression was disrupted. Transcriptomic profiling indicated that upregulated genes were enriched in cell-cell tight junctions, while downregulated genes were associated with oxygen binding, oxidative stress, stromal differentiation, and vascular development. Cross-species comparison with cloned mice suggested conserved genetic mechanisms underlying placental defects. These findings provide a crucial theoretical foundation for elucidating the mechanisms of placental failure in animal cloning and for developing strategies to enhance its efficiency.