The circRNA circ-Nbea participates in regulating diabetic encephalopathy.

Circular RNAs (circRNAs) play key roles in various pathogenic and biological processes in human disease. However, the effect of circRNAs on the development of diabetic encephalopathy (DE) remains largely unknown. Therefore, the aim of this study was to investigate changes in the expression of circRNAs and their potential mechanism in DE formation. Compared with db/m mice, spatial learning/memory, dendritic spines, and synaptic plasticity were all impaired in the hippocampus of the db/db mice. In addition, the dendritic spine density of neurons was significantly decreased after treatment with advanced glycation end-products (AGEs). We used high-throughput RNA sequencing (RNA-Seq) to detect circRNA expression in DE, and the results revealed that 183 circRNAs were significantly altered in primary hippocampal neurons treated with AGEs. Three circRNAs were chosen for detection using quantitative real-time polymerase chain reaction (qRT-PCR), including circ-Smox (chr2: 131511984-131516443), circ-Nbea (mmu-chr3: 56079859-56091120), and circ-Setbp1 (chr18: 79086551-79087180), and circ-Nbea expression was significantly decreased. According to the bioinformatics prediction and detection using qRT-PCR and double luciferase assays, circ-Nbea sponges miR-128-3p. Based on these results, we speculated that a newly identified circRNA, circ-Nbea, may play an important role in the development of DE, and the mechanism is mediated by sponging miR-128-3p. This study provides new insight into the treatment of DE.

miR-1247-3p mediates apoptosis of cerebral neurons by targeting caspase-2 in stroke.

Brain stroke is one of the leading causes of death worldwide. We explored a potential stroke-related role for a newly found microRNA, miR-1247-3p, and one of its target genes, caspase-2, predicted by TargetScanVert. In the present study, we found that miR-1247-3p was downregulated during ischemia/reperfusion (I/R) and that LV-miR-1247-3p overexpression attenuated brain impairment induced by I/R. Similar results were observed in neuro2a (N2a) cells treated with oxygen-glucose deprivation/reoxygenation (OGD/R). Caspase-2 was upregulated in the I/R and OGD/R model, while Z-VDVAD-FMK - the inhibitor of caspase-2-inhibited apoptosis of N2a cells induced by OGD/R. An miR-1247-3p mimic inhibited caspase-2 expression and attenuated apoptosis of N2a cells induced by OGD/R. Myocardin-related transcription factor-A (MRTF-A) overexpression upregulated miR-1247 and mature miR-1247-3p levels and attenuated apoptosis induced by OGD/R, whereas its anti-apoptotic function could be blocked by a miR-1247-3p inhibitor. Hence, we conclude that miR-1247-3p may protect cells during brain stroke. This study offers insights for the development of effective therapeutics for promoting the survival of cerebral neurons during brain I/R injury.