Mir-24 reduces serum lipid levels and inhibits brain tissue cells apoptosis of rats with cerebral infarction

Abstract

AIM: To study miR-24 effects on cerebral infarction in rats. MATERIAL and METHODS: A rat middle cerebral artery occlusion model (MCAO) was constructed. Intracerebroventricular stereotactic injection of miR-24 agomir/antagomir was performed in the rat MCAO model. According to different experiences, rats were divided into normal, sham, MCAO, miR-24 agomir and miR-24 antagomir groups. Serum TCH, HDL and TG levels were detected. RESULTS: Comparingthe normal and sham groups, we observed decreased relative miR-24 expression (P< 0.05) and increased cerebral infarction area percentage, apoptotic cells and relative caspase-3 protein expression (P< 0.05) in theMCAO, miR-24 agomirand miR-24 antagomir groups. TC, TG and HDL-C levels of the MCAO and miR-24 antagomir groups were higher than those of normal and sham groups (P< 0.05).Compared with the MCAO group, increased relative miR-24 expression (P< 0.05) and decreased TC, TG and HDL-C levels,cerebral infarction area percentage, number of apoptotic cells and caspase-3 expression (P< 0.05) were found in themiR-24 agomir group, contrasting with theobservations from the miR-24 antagomir group. CONCLUSION: miR-24 reduced serum TCH, HDL and TG levels and inhibited brain tissue cell apoptosis in rats with cerebral infarction.

Non-Coding RNA Regulatory Network in Ischemic Stroke

“…At present, many studies have shown that caspase is abnormally expressed in IS and regulated by multiple miRNAs (58). For example, miR-let-tc-3p, miR-195, miR-24, miR-233, miR-503, etc., have been proved to be related to this process (17,(26)(27)(28)59). miR-130a was upregulated in brain tissue of MCAO rats (60) and X-Linked Inhibitor Of Apoptosis (XIAP) was identified as its target molecule.…”

ISGylation is induced in neurons by demyelination driving ISG15-dependent microglial activation

“…These included miR-15b [69]; miR-23a/b and miR-27a [70][71][72][73]; miR-126a [74][75][76]; miR24, miR-26a, miR-149 [77][78][79][80][81][82][83][84]; and miR-365 [85]. Additionally, several of these upregulated mi-RNA transcripts have also been shown to be neuroprotective including miRNA 23a, miR-23b, miR-24, and miR-27a [86][87][88][89][90][91][92][93][94][95][96][97][98][99][100][101]. Finally, EVs from ISG15 knockdown neurons exhibited downregulation of several mi-RNA transcripts that have been shown to promote microglial or macrophage activation and cytokine secretion or neuronal toxicity (Fig.…”

“…Additionally, several of these upregulated mi-RNA species have been shown to be neuroprotective. For example, miRNA 23a, miR-23b, miR-24, and miR-27a are known to target APAF1 and pro-apoptotic BCL family proteins and thereby prevent neuronal apoptosis, and downregulation of these miRNAs during acute EAE, TBI, spinal cord injury, and stroke is thought to contribute to neuron and neurite loss [86][87][88][89][90][91][92][93][94][95][96][97][98]. Direct protection of neurons has been shown for miR-23a in spinal muscular atrophy [99] and for miR-27a in EAE and TBI by, respectively, reducing excitotoxicity through suppression of glutamate receptor subunits [168] and reducing oxidative injury by suppressing FOXO1 and FOXO3a [100,101].…”