Makori N, Peterson P E, Blankenship T N, Dillard-Telm L, Hummler H, Hendrickx A G
California Regional Primate Research Center, University of California, Davis 95616, USA.
J Med Primatol. 1998 Aug;27(4):210-9. doi: 10.1111/j.1600-0684.1998.tb00073.x.
Hindbrain and craniofacial development during early organogenesis was studied in normal and retinoic acid-exposed Macaca fascicularis embryos. 13-cis-retinoic acid impaired hindbrain segmentation as evidenced by compression of rhombomeres 1 to 5. Immunolocalization with the Hoxb-1 gene product along with quantitative measurements demonstrated that rhombomere 4 was particularly vulnerable to size reduction. Accompanying malformations of cranial neural crest cell migration patterns involved reduction and/or delay in pre- and post-otic placode crest cell populations that contribute to the pharyngeal arches and provide the developmental framework for the craniofacial region. The first and second pharyngeal arches were partially fused and the second arch was markedly reduced in size. The otocyst was delayed in development and shifted rostrolaterally relative to the hindbrain. These combined changes in the hindbrain, neural crest, and pharyngeal arches contribute to the craniofacial malformations observed in the retinoic acid malformation syndrome manifested in the macaque fetus.
在正常和暴露于视黄酸的食蟹猴胚胎中研究了早期器官发生过程中的后脑和颅面发育。13-顺式视黄酸损害后脑节段化，菱脑节1至5受压证明了这一点。用Hoxb-1基因产物进行免疫定位并结合定量测量表明，菱脑节4特别容易出现尺寸减小。伴随的颅神经嵴细胞迁移模式畸形包括耳前和耳后基板嵴细胞群减少和/或延迟，这些细胞群有助于咽弓并为颅面区域提供发育框架。第一和第二咽弓部分融合，第二弓尺寸明显减小。耳囊发育延迟，并相对于后脑向 rostrolaterally 移位。后脑、神经嵴和咽弓的这些综合变化导致了在猕猴胎儿中表现出的视黄酸畸形综合征中观察到的颅面畸形。
