School of Life Sciences, Tsinghua University, Beijing, 100084, China.
Shenzhen Key Lab of Health Science and Technology, Division of Life Science & Health, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.
Sci Rep. 2017 Jul 13;7(1):5270. doi: 10.1038/s41598-017-05560-1.
Diabetes is an inflammatory disease. Inflammation plays an important role in islet functions. However, the exact mechanisms by which inflammation affects islet functions remain unclear. In this study, we investigated the regulatory effects of miR-30a on inflammation and islet functions. The results indicate that miR-30a serves as an inflammation-resolving buffer factor by targeting interleukin 1a (IL-1α) in immune cells and in islet cells, which might play an important role in inflammation homeostasis. miR-30a ameliorates islet functions in an inflammatory micro-environment by targeting the IL-1α/nuclear factor kappa B (NFKB) p65 subunit (p65)/p62 (SQSTM1)/insulin axis, which can be developed into a novel antidiabetic approach. miR-30a serves as a promising inflammation-response biomarker in inflammatory diseases and is possibly activated by the toll-like receptor 4 (TLR4)/IL-1α/NFKB pathways. However, the exact molecular mechanisms by which miR-30a regulates inflammation and islet functions as well as the potential applications in transitional medicine require further elucidation.
糖尿病是一种炎症性疾病。炎症在胰岛功能中起着重要作用。然而，炎症影响胰岛功能的确切机制尚不清楚。在这项研究中，我们研究了 miR-30a 对炎症和胰岛功能的调节作用。结果表明，miR-30a 通过在免疫细胞和胰岛细胞中靶向白细胞介素 1a（IL-1α），充当炎症解决缓冲因子，这可能在炎症稳态中发挥重要作用。miR-30a 通过靶向白细胞介素 1α/核因子 kappa B（NFKB）p65 亚基（p65）/p62（SQSTM1）/胰岛素轴改善炎症微环境中的胰岛功能，这可能成为一种新的抗糖尿病方法。miR-30a 可作为炎症性疾病中炎症反应的有前途的生物标志物，并且可能通过 Toll 样受体 4（TLR4）/IL-1α/NFKB 途径被激活。然而，miR-30a 调节炎症和胰岛功能的确切分子机制以及在转化医学中的潜在应用仍需要进一步阐明。
