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鸡胚颅骨的软骨生成潜能:I. 低钙水平允许软骨分化。

Chondrogenic potential of chick embryonic calvaria: I. Low calcium permits cartilage differentiation.

作者信息

Jacenko O, Tuan R S

机构信息

Department of Biology, University of Pennsylvania, Philadelphia 19104.

出版信息

Dev Dyn. 1995 Jan;202(1):13-26. doi: 10.1002/aja.1002020103.

DOI:10.1002/aja.1002020103
PMID:7703518
Abstract

Calvaria from day-14 calcium-deficient chick embryos produced by long-term maintenance in shell-less culture, exhibit a cartilage-like phenotype (Jacenko and Tuan [1986] Dev. Biol. 115:215-232), which is restored to an osteogenic phenotype upon calcium repletion to the embryo. The expression of cartilage markers in a typically osteogenic tissue under calcium deficiency implies the presence of chondrogenic cells, and questions the conditions associated with calcium deficiency which may cause their divergent pathway of differentiation. In the present study, by explanting normal and shell-less embryonic calvarial pairs in organ culture in vitro and experimentally regulating their calcium supply, the calcium status of the calvaria was modulated as a function of medium calcium. Histological and immunoblotting analyses demonstrated for the first time that calvaria possess cells which can form genuine cartilage. This chondrogenic potential is expressed only in a low-calcium environment, where cartilage forms in both normal and shell-less calvarial pairs; their calcium-supplemented counterparts, however, develop as fully osteogenic tissues. Furthermore, chondrogenesis in both normal and shell-less calvaria indicates that the chondrogenic cells must be endogenous constituents of the calvaria, rather than being derived elsewhere in response to systemic calcium deficiency. Finally, the correlation between matrix under-calcification and cartilage expression in the embryonic calvarium suggests that calcium, perhaps in the form of matrix mineral, may modulate cell differentiation during skeletogenesis.

摘要

通过无壳培养长期维持产生的14日龄缺钙鸡胚的颅盖骨呈现出软骨样表型(雅琴科和段 [1986]《发育生物学》115:215 - 232),当胚胎补充钙后,该表型恢复为成骨表型。在缺钙情况下典型的成骨组织中软骨标记物的表达意味着存在软骨形成细胞,并对与缺钙相关的可能导致其分化途径不同的条件提出了疑问。在本研究中,通过在体外器官培养中移植正常和无壳胚胎颅盖骨对,并实验性地调节它们的钙供应,颅盖骨的钙状态作为培养基钙的函数被调节。组织学和免疫印迹分析首次证明颅盖骨拥有能够形成真正软骨的细胞。这种软骨形成潜能仅在低钙环境中表达,在正常和无壳颅盖骨对中都会形成软骨;然而,补充钙的对应物则发育为完全成骨的组织。此外,正常和无壳颅盖骨中的软骨形成表明软骨形成细胞必定是颅盖骨的内源性成分,而不是因全身缺钙而从其他地方衍生而来。最后,胚胎颅盖骨中基质钙化不足与软骨表达之间的相关性表明,钙,可能是以基质矿物质的形式,在骨骼发生过程中可能调节细胞分化。

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