<p>MicroRNA-579-3p Exerts Neuroprotective Effects Against Ischemic Stroke via Anti-Inflammation and Anti-Apoptosis</p>

Abstract

Background/Aims: Multiple studies have found that microRNAs (miRNAs) are involved in the development of cerebral ischemia. MiR-579-3p can inhibit inflammatory responses and apoptosis, leading to ischemia/reperfusion (I/R) damage. However, the mechanism of how miR-579-3p actions in brain I/R injury remains unclear. This study aimed to investigate the mechanism of the role of miR-579-3p in brain I/R injury. Methods: A rat model of cerebral ischemia-reperfusion injury was established by suture method. The effects of miR-579-3p on cerebral infarction size, brain water content, and neurological symptoms were evaluated. Flow cytometry was used to detect apoptosis. ELISA was used to detect the level of inflammatory factors. Western blot was used to detect the expression of P65, NCOA1, Bcl-2 and Bax. The relationship between miR-579-3p and NCOA1 was analyzed by bioinformatics analysis and luciferase assay. Results: Overexpression of miR-579-3p reduced infarct volume, brain water content and neurological deficits. Overexpression of miR-579-3p inhibited the expression level of the inflammatory cytokines, such as TNF-α, IL-6, COX-2 and iNOS, and increased the expression level of IL-10. MiR-579-3p overexpression inhibited NF-кB activity by reducing NRIP1. In addition, miR-579-3p could reduce the apoptotic rate of cortical neurons. Overexpression of miR-579-3p inhibited the activity of caspase-3, increased the expression level of anti-apoptotic gene Bcl-2 in neurons, and decreased the expression level of apoptotic gene Bax. Conclusion: miR-579-3p can be used to treat brain I/R injury, and its neuroprotective effect may be ascribed to the reduction of inflammation and apoptosis.

RETRACTED: Overexpression of circRNA circUCK2 Attenuates Cell Apoptosis in Cerebral Ischemia-Reperfusion Injury via miR-125b-5p/GDF11 Signaling

“…Increasing evidence has suggested that circRNAs are abundant in miRNA-binding sites, which play a role in the adsorption of miRNA in cells and block or reduce the inhibitory effect of miRNA on genes, thereby promoting the expression of target genes. 37 , 38 , 39 For instance, circSLC8A1 was reported to bind miR-130b/miR-494, which regulated bladder cancer progression. 40 Another study showed that circRNA DLGAP4 inhibited miR-143 activity in order to decrease the size of infarct areas and attenuate neuronal deficits and blood-brain barrier (BBB) damage in MCAO mice.…”

Oxytocin Receptor Signaling in Vascular Function and Stroke

“…Another current strategy to improve outcomes post-ischemia is the enhancement of cell survival through inhibiting apoptosis (Caglayan et al, 2019;Chen et al, 2020;Jia et al, 2020), reducing excitotoxicity (Maiolino et al, 2019;Jia et al, 2020), and improving metabolism (Ren et al, 2008). The general measures of reduced apoptosis are taken as a reduction in caspase activation and a higher ratio of Bcl-2 to Bax (Chen et al, 2020;Jia et al, 2020). Combatting excitotoxicity often ultimately focuses either on reducing glutamate signaling, mostly through NMDA receptors, or reducing intracellular calcium accumulation and waves in connected cells (Maiolino et al, 2019;Pietrogrande et al, 2019).…”

Circular RNA hsa_circ_0033144 (CircBCL11B) regulates oral squamous cell carcinoma progression via the miR-579/LASP1 axis

“…In addition, miR-579 was reported to form a complex with miR-221, miR-125b and specific RNA-binding proteins (RBPs) to target 3ʹUTR of TNFα mRNA, which impairs the protein synthesis by interfering with the translation [14]. Aberrant expression of miR-579 has been also reported in a variety of tumors and diseases [15][16][17], however, its potential involvement in oral squamous cell carcinoma (OSCC) remains to be studied. In this study, we evaluated the biological role and survey the molecular mechanism of circBCL11B in OSCC.…”