Lorenzini Antonello, Tresini Maria, Mawal-Dewan Madhu, Frisoni Lorenza, Zhang Hong, Allen Robert G, Sell Christian, Cristofalo Vincent J
The Lankenau Institute for Medical Research, 100 Lancaster Avenue, Wynnewood, PA 19096, USA.
Exp Gerontol. 2002 Oct-Nov;37(10-11):1149-56. doi: 10.1016/s0531-5565(02)00133-x.
Replicative senescence is characterized by numerous phenotypic alterations including loss of proliferative capacity and numerous changes in gene expression such as impaired serum inducibility of the immediate early gene c-fos and increased expression of collagenase. Transcription of c-fos in response to mitogens depends on the activation of a multiprotein complex formed on the c-fos serum response element (SRE), which includes the transcription factors serum response factor (SRF) and ternary complex factor (TCF). TCF is activated after phosphorylation by the Extracellular signals Regulated Kinase 1 and 2 (ERK1/2), two kinases of the Raf/MEK/ERK signaling pathway. We have previously demonstrated that collagenase expression is under positive regulation by the transcription factor FKHRL1 and that this transcription factor is under negative regulation by the phosphatidylinositol 3-kinase(PI3K)/Akt(PKB) pathway. Although total activity of ERK and Akt was similar in total cell lysates from early and late passage fibroblasts our data indicate that in senescent cells neither ERK nor Akt are able to phosphorylate efficiently their nuclear targets. Our findings suggest that although they can be fully activated in the cytosol of both early and late passage cells, the Raf/MEK/ERK and the PI3K/Akt pathways, which are essential for cellular proliferation, are down regulated in the nuclei of senescent cells.
复制性衰老的特征是众多表型改变,包括增殖能力丧失以及基因表达的大量变化,如即刻早期基因c-fos的血清诱导性受损和胶原酶表达增加。c-fos对有丝分裂原的转录依赖于在c-fos血清反应元件(SRE)上形成的多蛋白复合物的激活,该复合物包括转录因子血清反应因子(SRF)和三元复合物因子(TCF)。TCF在被细胞外信号调节激酶1和2(ERK1/2)磷酸化后被激活,ERK1/2是Raf/MEK/ERK信号通路的两种激酶。我们之前已经证明胶原酶的表达受转录因子FKHRL1的正调控,并且该转录因子受磷脂酰肌醇3激酶(PI3K)/Akt(PKB)通路的负调控。尽管早期和晚期传代成纤维细胞的总细胞裂解物中ERK和Akt的总活性相似,但我们的数据表明,在衰老细胞中,ERK和Akt都不能有效地磷酸化它们的核靶点。我们的研究结果表明,尽管Raf/MEK/ERK和PI3K/Akt通路在早期和晚期传代细胞的细胞质中都能被完全激活,但对于细胞增殖至关重要的这两条通路在衰老细胞的细胞核中被下调。