Methyltransferase-like protein 3 (METTL3) mediated N6-Methyladenosine (m 6 A) modification has been implicated in many physiological and pathological processes. However, its function and mechanism in kidney aging are not entirely clear. Here, we investigated changes in m 6 A levels of aging kidneys and the role of METTL3 in senescent renal tubular epithelial cells and its potential mechanisms. First, we used the naturally aged mouse model and the D -galactose ( D -gal)-induced aged mouse model. Dot blot and m 6 A RNA methylation quantification showed significantly decreased m 6 A levels in both models. In addition, we observed that METTL3 was down-regulated in D -gal-induced senescent human renal tubular epithelial cell line (HK-2). METTL3 reduction was associated with senescence-related phenotypes of HK-2 cells. We also found that miR-181a-5p attenuated HK-2 senescence by targeting the NF-κB pathway. Moreover, METTL3 was able to promote the maturation of miR-181a-5p and then inhibited the expression of NF-κB and IL-1α. Taken together, we demonstrate that the METTL3/miR-181a-5p/NF-κB axis counteracts HK-2 senescence. Our results suggest that METTL3 may be a novel biomarker and a potential therapy target for kidney aging.
文章引用产品列表
-
- CCS012
- 周期试剂盒
Cell Cycle Staining Kit 细胞周期检测试剂盒
- ¥390.00
