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在体外暴露于上皮细胞和甲状腺素的胚胎鸡的梅克尔软骨中,软骨细胞肥大或骨生成的缺失。

Lack of either chondrocyte hypertrophy or osteogenesis in Meckel's cartilage of the embryonic chick exposed to epithelia and to thyroxine in vitro.

作者信息

Kavumpurath S, Hall B K

机构信息

Department of Biology, Dalhousie University, Halifax, Nova Scotia, Canada.

出版信息

J Craniofac Genet Dev Biol. 1990;10(3):263-75.

PMID:2262537
Abstract

Osteogenesis was not initiated when Meckel's cartilages from embryonic chicks of Hamburger and Hamilton (H. H.) stages 38 and 39 were recombined with mandibular epithelia obtained from embryos of H. H. stage 22 (a stage when an epithelial-mesenchymal interaction elicits osteogenesis from mandibular mesenchyme) and grafted to the chorioallantoic membranes of host embryos for 7 to 21 days. Failure of osteogenesis was not because the cartilage inhibited or blocked the osteogenesis-initiating capabilities of mandibular epithelium for mandibular epithelia could still elicit osteogenesis when removed from Meckel's cartilages and recombined with mandibular mesenchyme. Chondrocyte hypertrophy is associated with osteogenesis in other cartilages, including Meckel's cartilage from rodent embryos. However, Meckel's cartilages from chick embryos of H. H. stages 34, 38, and 39 failed to hypertrophy when cultured in the presence of 7.5 nM thyroxine (3,3',5-triiodo-L-thyroxine), although H. H. stage 28 tibial chondrocytes cocultured with Meckel's cartilage did hypertrophy. Therefore, avian Meckelian chondrocytes fail to hypertrophy or to produce osteoprogenitor cells in response to stimuli known to evoke these events in other skeletal cells.

摘要

当将处于汉伯格和汉密尔顿(H. H.)38期和39期的胚胎小鸡的梅克尔软骨,与取自H. H. 22期胚胎(此阶段上皮-间充质相互作用可引发下颌间充质骨生成)的下颌上皮重组,并移植到宿主胚胎的尿囊绒毛膜上7至21天时,骨生成并未启动。骨生成失败并非因为软骨抑制或阻碍了下颌上皮启动骨生成的能力,因为当从梅克尔软骨中取出并与下颌间充质重组时,下颌上皮仍能引发骨生成。软骨细胞肥大与其他软骨(包括啮齿动物胚胎的梅克尔软骨)的骨生成相关。然而,当在7.5 nM甲状腺素(3,3',5-三碘-L-甲状腺素)存在的情况下培养时,H. H. 34期、38期和39期的小鸡胚胎的梅克尔软骨未能肥大,尽管与梅克尔软骨共培养的H. H. 28期胫骨软骨细胞确实肥大。因此,禽类梅克尔软骨细胞不会因已知能在其他骨骼细胞中引发这些事件的刺激而肥大或产生骨祖细胞。

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