Zyuz'kov G N, Danilets M G, Ligacheva A A, Zhdanov V V, Udut E V, Miroshnichenko L A, Simanina E V, Chaikovskii A V, Trofimova E S, Minakova M Yu, Udut V V, Dygai A M
Research Institute of Pharmacology, Siberian Division of the Russian Academy of Medical Sciences, Tomsk, Russia,
Bull Exp Biol Med. 2014 Aug;157(4):436-9. doi: 10.1007/s10517-014-2584-z. Epub 2014 Aug 12.
We studied PI3K, MAPK/EPK1/2 and p38-dependent signaling cascade under stimulation of the functions of mesenchymal progenitor cells by fibroblast growth factor. The important role of PI3K and EPK1/2 in the realization of their growth potential has been revealed. Experiments have demonstrated a blocking effect of PI3K inhibitor on proliferation and differentiation of progenitor cells and EPK1/2 inhibitor on mitotic activity of the progenitor cells. The p38-mediated MAPK pathway did not play a role in determining the proliferative and differentiation status of fibroblast CFU.
我们研究了在成纤维细胞生长因子刺激间充质祖细胞功能的情况下,磷脂酰肌醇-3激酶(PI3K)、丝裂原活化蛋白激酶/细胞外信号调节激酶1/2(MAPK/EPK1/2)和p38依赖的信号级联反应。已揭示PI3K和EPK1/2在实现其生长潜能中发挥的重要作用。实验证明PI3K抑制剂对祖细胞的增殖和分化具有阻断作用,而EPK1/2抑制剂对祖细胞的有丝分裂活性具有阻断作用。p38介导的MAPK途径在决定成纤维细胞集落形成单位(CFU)的增殖和分化状态方面不起作用。