College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
Acta Biochim Biophys Sin (Shanghai). 2021 Jan 12;53(1):36-45. doi: 10.1093/abbs/gmaa145.
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.
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。