METTL3 contributes to renal ischemia-reperfusion injury by regulating Foxd1 methylation.

METTL3 contributes to renal ischemia-reperfusion injury by regulating Foxd1 methylation. Am J Physiol Renal Physiol. 2020 Sep 21;: Authors: Meng F, Liu Y, Chen Q, Ma Q, Gu S, Cui R, Cao R, Zhao M Abstract To investigate the mechanism of renal ischemia-reperfusion injury (IRI) via the regulation of N6-methyl-adenosine (m6A) and relevant genes, IRI was induced in Sprague Dawley rats and the urine and serum creatinine levels and tissue structure changes were observed. m6A and METTL3 protein levels were assessed via dot blotting and western blotting, respectively. The hypoxia/reoxygenation (H/R) cell model was constructed using NRK-52E cells, and METTL3 protein levels were assessed. METTL3 was inhibited to observe its impact on NRK-52E cell apoptosis and m6A expression in H/R processes. Methylated RNA immunoprecipitation (MeRIP) sequencing was conducted, followed by MeRIP-qRT-PCR and qRT-PCR validation. Our results indicated that urine and serum creatinine levels increased and that renal injury and cell apoptosis were both observed in IRI model. In additon, m6A expression increased in the IRI model, and METTL3 protein levels significantly increased in the IRI and H/R models. When METTL3 was inhibited, the m6A levels were accordingly decreased and cell apoptosis was suppressed in the H/R in vitro model. Based on MeRIP sequencing, tfap2a, cyp1b1, and foxd1 were significantly differentially expressed, as was m6A, which is involved in the ne...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research