MCAM 敲低会损害 PPARγ 的表达和 3T3-L1 成纤维细胞向脂肪细胞的分化。
MCAM knockdown impairs PPARγ expression and 3T3-L1 fibroblasts differentiation to adipocytes.
机构信息
Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Pabellón 2, Ciudad Universitaria, 1428, Buenos Aires, Argentina.
Universidad de Buenos Aires, CONICET, Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales (IQUIBICEN), Buenos Aires, Argentina.
出版信息
Mol Cell Biochem. 2018 Nov;448(1-2):299-309. doi: 10.1007/s11010-018-3334-8. Epub 2018 Feb 21.
We investigated for the first time the expression of melanoma cell adhesion molecule (MCAM) and its involvement in the differentiation of 3T3-L1 fibroblasts to adipocytes. We found that MCAM mRNA increased subsequent to the activation of the master regulator of adipogenesis, PPARγ, and this increase was maintained in the mature adipocytes. On the other hand, MCAM knockdown impaired differentiation and induction of PPARγ as well as expression of genes activated by PPARγ. However, events that precede and are necessary for early PPARγ activation, such as C/EBPβ induction, β-catenin downregulation, and ERK activation, were not affected in the MCAM knockdown cells. In keeping with this, the increase in PPARγ mRNA that precedes MCAM induction was not altered in the knockdown cells. In conclusion, our findings suggest that MCAM is a gene upregulated and involved in maintaining PPARγ induction in the late but not in the early stages of 3T3-L1 fibroblasts adipogenesis.
我们首次研究了黑色素瘤细胞黏附分子（MCAM）的表达及其在 3T3-L1 成纤维细胞向脂肪细胞分化中的作用。我们发现，MCAM mRNA 在脂肪生成的主调控因子 PPARγ 激活后增加，并且在成熟脂肪细胞中保持增加。另一方面，MCAM 敲低会损害分化和 PPARγ 的诱导以及 PPARγ 激活的基因的表达。然而，在 MCAM 敲低细胞中，早期 PPARγ 激活所必需的事件，如 C/EBPβ诱导、β-连环蛋白下调和 ERK 激活，不受影响。与此一致的是，在诱导 MCAM 之前增加的 PPARγ mRNA 在敲低细胞中没有改变。总之，我们的发现表明，MCAM 是一种上调基因，参与维持 3T3-L1 成纤维细胞脂肪生成晚期而非早期的 PPARγ 诱导。
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