ArticleExperimental and therapeutic medicine2020
MicroRNA-1236-3p/translationally controlled tumor protein (TPT1) axis participates in congenital hypothyroidism progression by regulating neuronal apoptosis.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- The role of miRNA-624-5p in congenital hypothyroidism and its molecular mechanism by targeting SIRT1.Genes & genomics · 2022Article
- Role of sirtuin 1 in the brain development in congenital hypothyroidism rats via the regulation of p53 signaling pathway.Bioengineered · 2022Article
- MicroRNA-489-3p plays a significant role in congenital hypothyroidism through regulating neuronal cell apoptosis via targeting translationally controlled tumor protein 1.Experimental and therapeutic medicine · 2021Article
Corrections and comments
- Retracted
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 results revealed that miR-1236-3p expression was significantly upregulated, whilst TPT1 expression was significantly downregulated in the hippocampus tissues of CH rats compared with the control group. TPT1 was confirmed as a target of miR-1236-3p. MiR-1236-3p inhibitor prevented hippocampal neuron apoptosis induced by CH induction, which was reversed by TPT1-siRNA transfection. In addition, following miR-1236-3p inhibitor transfection, neuronal cell apoptosis significantly reduced compared with the control group, which was accompanied by significantly increased expressions of Pim-3, p-Bad (Ser112) and Bcl-xL expression. These effects were reversed by TPT1-siRNA co-transfection. These results indicated that inhibition of miR-1236-3p expression inhibited neuron apoptosis
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