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miR-199b-5p 通过靶向 Fzd6 调控 Wnt 信号通路增强骨髓胸腺上皮细胞的增殖。

miR-199b-5p enhances the proliferation of medullary thymic epithelial cells via regulating Wnt signaling by targeting Fzd6.

机构信息

College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.

出版信息

Acta Biochim Biophys Sin (Shanghai). 2021 Jan 12;53(1):36-45. doi: 10.1093/abbs/gmaa145.

Abstract

Thymic epithelial cells (TECs) are essential regulators of T-cell development and selection. miRNAs play critical roles in regulating TEC proliferation during the process of thymic aging. Our previous studies revealed that miR-199b-5p was upregulated in TECs from 1- to 3-month-old mice. But its function and potential mechanism are not clear. We hypothesized that miR-199b-5p may play an important role in age-related thymus involution via targeting some genes. To confirm it, the murine thymic epithelial cell line 1 (MTEC1) cells were used. Our results showed that overexpression of miR-199b-5p can enhance MTEC1 cell proliferation. On the contrary, repression of miR-199b-5p can inhibit MTEC1 cell proliferation. Meanwhile, it was confirmed that frizzled receptor 6 (Fzd6) is the direct target gene of miR-199b-5p. Furthermore, overexpression of miR-199b-5p can upregulate the expressions of β-catenin, Tcf7, Wnt4, and C-myc to activate Wnt signaling and cell cycle signaling. Silence of Fzd6 and co-transfection with siFzd6 and miR-199b-5p mimic/inhibitor confirmed that the biological function of miR-199b-5p is indeed by targeting Fzd6 in medullary TECs. Overall, miR-199b-5p is an important regulator in medullary TEC proliferation through targeting Fzd6 to activate Wnt signaling and cell cycle signaling. Our data indicate that miR-199b-5p may block the process of thymic aging and be a potential therapeutic target for thymus involution.

摘要

胸腺上皮细胞(TEC)是 T 细胞发育和选择的重要调节者。miRNA 在调节胸腺衰老过程中的 TEC 增殖中发挥关键作用。我们之前的研究表明,miR-199b-5p 在 1-3 个月大的小鼠的 TEC 中上调。但其功能和潜在机制尚不清楚。我们假设 miR-199b-5p 可能通过靶向某些基因在与年龄相关的胸腺萎缩中发挥重要作用。为了证实这一点,使用了小鼠胸腺上皮细胞系 1(MTEC1)细胞。我们的结果表明,miR-199b-5p 的过表达可以增强 MTEC1 细胞的增殖。相反,miR-199b-5p 的抑制可以抑制 MTEC1 细胞的增殖。同时,证实 frizzled 受体 6(Fzd6)是 miR-199b-5p 的直接靶基因。此外,miR-199b-5p 的过表达可以上调β-catenin、Tcf7、Wnt4 和 C-myc 的表达,激活 Wnt 信号和细胞周期信号。Fzd6 的沉默和共转染 siFzd6 和 miR-199b-5p 模拟物/抑制剂证实,miR-199b-5p 的生物学功能确实是通过靶向髓质 TEC 中的 Fzd6 来实现的。总体而言,miR-199b-5p 通过靶向 Fzd6 激活 Wnt 信号和细胞周期信号,是髓质 TEC 增殖的重要调节因子。我们的数据表明,miR-199b-5p 可能阻止胸腺衰老过程,是胸腺萎缩的潜在治疗靶点。

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