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Activating enhancer binding protein 2 epsilon (AP-2ε)-deficient mice exhibit increased matrix metalloproteinase 13 expression and progressive osteoarthritis development

机译:活化增强剂结合蛋白2 epsilon(AP-2ε)缺陷小鼠表现出增加的基质金属蛋白酶13表达和进行性骨关节炎的发展

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摘要

IntroductionThe transcription factor activating enhancer binding protein 2 epsilon (AP-2ε) was recently shown to be expressed during chondrogenesis as well as in articular chondrocytes of humans and mice. Furthermore, expression of AP-2ε was found to be upregulated in affected cartilage of patients with osteoarthritis (OA). Despite these findings, adult mice deficient for AP-2ε (Tfap2e−/−) do not exhibit an obviously abnormal cartilaginous phenotype. We therefore analyzed embryogenesis of Tfap2e−/− mice to elucidate potential transient abnormalities that provide information on the influence of AP-2ε on skeletal development. In a second part, we aimed to define potential influences of AP-2ε on articular cartilage function and gene expression, as well as on OA progression, in adult mice.
机译:引言最近发现转录因子激活增强子结合蛋白2 epsilon(AP-2ε)在软骨生成过程中以及在人和小鼠的关节软骨细胞中表达。此外,发现骨关节炎(OA)患者的受影响的软骨中AP-2ε的表达上调。尽管有这些发现,但缺乏AP-2ε(Tfap2e -/-)的成年小鼠并未表现出明显的软骨表型异常。因此,我们分析了Tfap2e -/-小鼠的胚胎发生,以阐明潜在的短暂异常,从而提供有关AP-2ε对骨骼发育影响的信息。在第二部分中,我们旨在确定AP-2ε对成年小鼠关节软骨功能和基因表达以及OA进展的潜在影响。

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