ArticleBMC molecular and cell biology2025
Targeting METTL16 attenuates mesangial cell viability and fibrosis in a high-glucose state by suppressing m6A modification and the expression of RAP1B.
Article in BMC molecular and cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMethyltransferase-like 16 (METTL16) is involved in regulating kidney disease progression. This study aimed to investigate the effect of METTL16 on the progression of diabetic kidney disease (DKD) and its potential mechanism.
methodsSV40-MES13 cells were transfected with METTL16 siRNA (siMETTL16), scramble control (siNC), or RAP1B siRNA (siRAP1B) under low glucose (LG) or high glucose (HG) conditions. Subsequently, RNA immunoprecipitation (RIP) assays, cell viability assays, EdU staining, TUNEL staining, ROS staining, and MDA detection were carried out.
resultsIn SV40-MES13 cells, cell viability, the number of EdU-positive cells, the MDA level, METTL16 mRNA, and protein levels were greater in the HG groups than in the control group. Moreover, cell viability, the number of EdU-positive cells, and VIMENTIN protein levels were lower, whereas the apoptosis rate and ROS and MDA levels were greater in the HG + siMETTL16 group than in the HG + siNC group. RAP1B mRNA and protein levels and N
conclusionMETTL16 knockdown attenuates cell viability and fibrosis by reducing m6A modification and the expression of RAP1B in high glucose-treated mesangial cells, suggesting the potential of METTL16 as a treatment target for DKD.
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