MicroRNA-1236-3p/translationally controlled tumor protein (TPT1) axis participates in congenital hypothyroidism progression by regulating neuronal apoptosis.

MicroRNA-1236-3p/translationally controlled tumor protein (TPT1) axis participates in congenital hypothyroidism progression by regulating neuronal apoptosis. Exp Ther Med. 2020 Jan;19(1):459-466 Authors: Meng T, Shen S, Li C, Liu X Abstract Congenital hypothyroidism (CH) is an endocrine disease caused by congenital thyroid hormone (TH) deficiency. MicroRNAs (miRNAs or miRs) have been reported to inhibit the progression of congenital hypothyroidism. However, the expression and role of miR-1236-3p in CH remains unclear. To address this, 12 day old Sprague-Dawley rats were divided into five groups: Control; Congenital hypothyroidism (CH), miR-1236-3p inhibitor control (inhibitor control); miR-1236-3p inhibitor (inhibitor); and miR-1236-3p inhibitor + translationally-controlled tumor protein 1 (TPT1)-small interfering (si)RNA (inhibitor + siRNA). Propylthiouracil (50 mg/day) was injected intraperitoneally into pregnant rats to generate pups with CH. The levels of miR-1236-3p and TPT1 were detected via reverse transcription-quantitative PCR and western blot analysis. Bioinformatics analysis was performed to predict the targets of miR-1236-3p, which was confirmed using dual luciferase reporter assay. Flow cytometry and MTT assay were used to measure neuronal cell apoptosis and cell viability, whereas western blotting was applied to detect the expression of Pim-3, p-Bad (Ser112), Bad and Bcl-xL, proteins associated with apoptosis. The resul...
Source: Experimental and Therapeutic Medicine - Category: General Medicine Tags: Exp Ther Med Source Type: research