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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Analysis of Variance, Animals, Baculoviral IAP Repeat-Containing 3 Protein, Brain, Brain Infarction, Cerebellar Nuclei, Deep Brain Stimulation, Disease Models, Animal, Gene Expression Regulation, In Situ Nick-End Labeling, Inhibitor of Apoptosis Proteins, Male, MicroRNAs, Mutation, Nervous System Diseases, Oligonucleotides, Antisense, RNA, Messenger, Rats, Rats, Sprague-Dawley, Stroke, bcl-2 Homologous Antagonist-Killer Protein.
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Does microRNA-29c correlate with Neuroprotection Induced by FNS by Targeting Both Birc2 and Bak1 in Rat Brain after Stroke? Context: Studies showed fastigial nucleus stimulation (FNS) reduced brain damage, but the mechanisms of neuroprotection induced by FNS were not entirely understood; MicroRNAs are noncoding RNA molecules that regulate gene expression in a posttranscriptional manner, but their functional consequence in response to ischemia-reperfusion (IR) remains unknown. We investigated the role of microRNA-29c in the neuroprotection induced by FNS in rat. The IR rat models were conducted 1 day after FNS. Besides, miR-29c antagomir (or agomir or control) was infused to the left intracerebroventricular 1 day before IR models were conducted. We detected differential expression of Birc2 mRNA (also Bak1mRNA and miR-29c) level among different groups by RT-qPCR. The differential expression of Birc2 protein (also Bak1 protein) level among different groups was surveyed via Western blot. The neuroprotective effects were assessed by infarct volume, neurological deficit, and apoptosis. MiR-29c was decreased after FNS. Moreover, miR-29c directly bound to the predicted 3'-UTR target sites of Birc2 and Bak1 genes. Furthermore, over-expression of miR-29c effectively reduced Birc2 (also Bak1) mRNA and protein levels, increased infarct volume and apoptosis, and deteriorated neurological outcomes, whereas down-regulation played a neuroprotective role.
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MiR-29c correlates with the neuroprotection induced by FNS by negatively regulating Birc2 and Bak1. Final Decision: yes