Cellular anomalies underlying retinoid-induced phocomelia.

摘要: The question of how alterations in cell behavior produced by retinoic acid (RA) influenced the development skeletogenic mesenchyme limb bud was examined this study. Our established model employed, which involves treatment pregnant mice with a teratogenic dose RA (100mg/kg) on 11 days postcoitum (dpc) resulting severe truncation all long bones forelimbs virtually every exposed fetus. It is shown that RA, administered at stage to induce phocomelia embryos, resulted immediate appearance enhanced death within central core bud, an area destined for chondrogenesis. mesenchyme, untreated buds experiences sharp decline proliferation heralding onset chondrogenesis, demonstrated reversal process; maintained higher rate upon exposure. These events and disorganization chondrogenic anlage, more pronounced zeugopodal than autopod. We conclude inhibition chondrogenesis secondary disruption cellular caused likely consequence misregulation growth factor signaling cascade.