Key Laboratory of Neuroscience, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China.
Institute of Neuroscience and The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China.
Int J Mol Med. 2018 Apr;41(4):2037-2049. doi: 10.3892/ijmm.2018.3418. Epub 2018 Jan 23.
Direct derivation of human induced pluripotent stem cells into neural precursor cells and differentiation of these into neurons holds great promise in the cell therapy of neurodegenerative diseases. However, the availability and survival rate of neurons requires improvement. In the present study, it was found that the addition of 5 ng/ml leukocyte inhibitory factor (LIF) during the process of differentiation significantly improved the expression of neuron‑specific class III β‑tubulin (TUJ1) and microtubule‑associated protein 2 (MAP2), as detected by immunofluorescence and western blotting. In addition, LIF improved the cell viability, increased the expression of phosphorylated‑protein kinase B (AKT), downregulated the expression of proinflammatory cytokines, including interleukin‑1α (IL‑1α) and tumor necrosis factor‑α (TNF-α), and upregulated the expression of anti‑inflammatory cytokines, including interleukin‑10 (IL‑10) and transforming growth factor‑β (TGF-β). After adding the phosphatidylinositol 3-kinase (PI3K)/AKT signaling inhibitor LY294002 or wortmannin to the LIF differentiation group, LIF-induced changes in the protein expression of TUJ1 and MAP2 were reversed, but this effect could not be prevented by rapamycin, a mechanistic target of rapamycin signaling inhibitor. The expression of cytokines associated with inflammation and cell viability was reversed by LY294002 and wortmannin, but not by rapamycin. In conclusion, LIF could improve neuronal differentiation and survival through the activation of PI3K/AKT signaling and the anti‑inflammatory effect. The anti‑inflammatory effect may be mediated by the activation of PI3K/AKT.
直接将人类诱导多能干细胞分化为神经前体细胞,并进一步分化为神经元,在神经退行性疾病的细胞治疗中具有广阔的应用前景。然而,神经元的可用性和存活率仍有待提高。本研究发现,在分化过程中添加 5ng/ml 白细胞抑制因子(LIF)可显著提高神经元特异性 III 类 β-微管蛋白(TUJ1)和微管相关蛋白 2(MAP2)的表达,通过免疫荧光和 Western blot 检测。此外,LIF 可提高细胞活力,增加磷酸化蛋白激酶 B(AKT)的表达,下调促炎细胞因子白细胞介素-1α(IL-1α)和肿瘤坏死因子-α(TNF-α)的表达,上调抗炎细胞因子白细胞介素-10(IL-10)和转化生长因子-β(TGF-β)的表达。在 LIF 分化组中加入磷脂酰肌醇 3-激酶(PI3K)/AKT 信号通路抑制剂 LY294002 或渥曼青霉素后,LY294002 可逆转 LIF 诱导的 TUJ1 和 MAP2 蛋白表达变化,但雷帕霉素(mTOR 信号通路抑制剂)不能阻断这一作用。LY294002 和渥曼青霉素可逆转与炎症和细胞活力相关的细胞因子的表达,但雷帕霉素不能。总之,LIF 可通过激活 PI3K/AKT 信号通路和抗炎作用来改善神经元的分化和存活。抗炎作用可能是通过激活 PI3K/AKT 来介导的。