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Cathepsin K Regulates Adipocyte Differentiation: Possible Involvement Of Type I Collagen Degradation

机译:组织蛋白酶K调节脂肪细胞分化:可能涉及I型胶原降解。

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We previously found that cathepsin K (CTSK) played an important role in adipocyte differentiation. However, the underlying molecular mechanism is not clear. Through the time window study, it was observed that CTSK activities were required mainly in the early phases of adipogenic process. At the same time, the expression of type I collagen disappeared. However, type I collagen can still be observed during the whole process when the CTSK inhibitor-E64 was added. The mRNA levels of peroxisome proliferator-activated receptor γ (PPAR-γ) and CCAAT/enhancer binding protein α (C/EBP-α) was also declining. These imply that CTSK may play a role in adipogenesis in early differentiation phases and produce an effect at least partly by degrading type I collagen, which may provides a basis for developing novel therapeutic approaches to treat obesity and the diseases associated with it.
机译:我们以前发现组织蛋白酶K(CTSK)在脂肪细胞分化中起重要作用。但是,潜在的分子机制尚不清楚。通过时间窗研究,观察到CTSK活性主要在成脂过程的早期阶段需要。同时,I型胶原蛋白的表达消失了。但是,在添加CTSK抑制剂-E64的整个过程中仍可以观察到I型胶原蛋白。过氧化物酶体增殖物激活受体γ(PPAR-γ)和CCAAT /增强子结合蛋白α(C /EBP-α)的mRNA水平也在下降。这些暗示CTSK可能在早期分化阶段中在脂肪形成中起作用,并且至少部分地通过降解I型胶原产生作用,这可以为开发治疗肥胖症及其相关疾病的新治疗方法提供基础。

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