Thrombospondin 2-null mice
Introduction Thrombospondin 2 (TSP2), a matricellular protein with a primary role in modulating cell matrix interactions, has been implicated in tissue repair and foreign body responses. Technology description TSP2-null mice were produced by targeted disruption of the thrombospondin 2 gene in embryonic stem cells by homologous recombination. Correctly targeted ES cells were microinjected into C57BL/6 mouse blastocysts and the resulting male chimeras were mated with C57BL/6 females. Agouti progeny were genotyped by Southern blot analysis of tail DNA. Heterozygous offspring were then bred to homozygosity. Subsequently, chimeras derived from both J1 and RW4 ES cells were mated with 129/SvJ females, and germline heterozygous animals were mated to produce homozygous TSP2-null mice in a homogeneous 129 background. TSP2-null mice display a complex phenotype characterized by abnormal connective tissues, increased vascular density, a bleeding diathesis, and increased bone growth. In addition, TSP2-null skin fibroblasts and wound granulation tissue display a two-fold increase in the level of matrix metalloproteinase (MMP)2. These mice are useful for studies of angiogenesis, tissue remodeling following injury, platelet biogenesis and function, bone growth, and regulation of MMP metabolism. Related Publication(s)
Journal of Cell biology 140(2):419-430, 1998.
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