Limb chondrogenesis is compromised in the versican deficient hdf mouse.
Limb chondrogenesis is compromised in the versican deficient hdf mouse.
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DOI:
10.1016/j.bbrc.2005.06.189
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发表时间:
2005-09
影响因子:
3.1
通讯作者:
Dennis R. Williams;Ashley R. Presar;A. Richmond;C. Mjaatvedt;S. Hoffman;A. A. Capehart-A.
中科院分区:
文献类型:
--
作者:
Dennis R. Williams;Ashley R. Presar;A. Richmond;C. Mjaatvedt;S. Hoffman;A. A. Capehart-A.
It has been suggested that the matrix proteoglycan, versican, may perform a functional role during early events of limb skeletogenesis largely by virtue of its spatiotemporal expression pattern in precartilage mesenchymal aggregations. The versican-deficient hdf transgenic mouse has provided the first model to explore the implications of a null mature versican on limb chondrogenesis. Due to lethality of hdf homozygous embryos prior to limb cartilage differentiation, high-density micromass cultures were employed to compare the chondrogenic capacity of hdf mutant limb mesenchyme to that of wild-type. In homozygous hdf mesenchyme, aggregation was severely compromised and neither cartilage-characteristic Type II collagen nor alcian blue positive foci were detected during a 6-day period of culture. Three-dimensional culture of hdf mutant mesenchyme, however, showed that in a permissive environment mutant cells also expressed Type II collagen. Results strongly suggest that mature versican proteoglycan is essential for precartilage aggregation and subsequent cartilage differentiation.