miR‑363‑3p attenuates the oxygen‑glucose deprivation/reoxygenation‑induced neuronal injury in vitro by targeting PDCD6IP

Abstract

The purpose of the present study was to explore the functional role of microrna (mir)-363-3p and related regulatory mechanisms in cerebral ischemia/reperfusion (i/r) injury. The neuronal cell line SH-SY5Y was exposed to 4 h of oxygen and glucose deprivation (oGd), followed by 6, 12, 24 and 48 h of re-oxygenation to mimic i/r injury in vitro. Cell viability, apoptosis and inflammation were assessed by ccK-8, lactate dehydrogenase (ldH), flow cytometry and eliSa assays. The association between mir-363-3p and programmed cell death 6-interacting protein (Pdcd6iP) was further confirmed using luciferase reporter assay. our data revealed that the expression level of miR-363-3p was significantly downregulated after oGd/r induction. overexpression of mir-363-3p markedly suppressed OGD/R-induced cell injury, as reflected by attenuated cell viability, reduced apoptosis, ldH activity and pro-inflammatory cytokine levels. Mechanistically, Pdcd6iP was confirmed as the target of mir-363-3p. Furthermore, Pdcd6iP knockdown imitated, while overexpression reversed the effects of mir-363-3p overexpression on oGd/r-induced cell injury. collectively, mir-363-3p could attenuate oGd/r-induced cell injury by alleviating apoptosis and inflammation, which may be mediated, at least in part, via inhibition of Pdcd6iP.

Hmgcs2 is the hub gene in diabetic cardiomyopathy and is negatively regulated by Hmgcs2, promoting high glucose‐induced cardiomyocyte injury

“…miR‐363 is a predictive, diagnostic, and prognostic biomarker for type 2 diabetes. 47 In addition, miR‐363 is able to suppress the pro‑inflammatory cytokine levels in cerebral ischemia/reperfusion injury 48 and moderate oxidative stress in the context of propofol‐induced neurotoxicity. 49 Our experimentation suggested miR‐363‐5p was downregulated in HG‐induced H9C2 cells and negatively regulated Hmgcs2, and miR‐363‐5p overexpression attenuated HG‐induced cell injury as evidenced by decreased LDH release, apoptosis, inflammation, and oxidative stress.…”

American Ginseng for the Treatment of Alzheimer’s Disease: A Review

“…Moreover, ginsenoside Rg1 has been observed to attenuate neuronal apoptosis by increasing the expression of miR-873-5p in AD [145]. We speculate that microRNAs involved in inducing apoptosis and attenuating neuronal damage, such as miR-466i-5p and miR-363-3p, may be potential targets for ginsenoside Rg1 in the treatment of AD; however, this requires further experimental validation [212,213]. On the other hand, ginsenoside Rg1 has been reported to increase ACh levels in a rat model of AD, which may be associated with its potential ability to penetrate the blood-brain barrier (BBB) and reach its target [180].…”

Circulating microRNA Profiles Identify a Patient Subgroup with High Inflammation and Severe Symptoms in Schizophrenia Experiencing Acute Psychosis

“…Nucleus pulposus cells (human) treated with LPS and miR-25b-3p inhibitor [47] Mesenchymal stem cell (mouse) treated with oxygen-glucose deprivation and miR-25-3p inhibitor [48] CTX TNA2 and serum (mouse) treated with LPS after transfected with miR-25-5p mimic [49] H9C2 cells (rat) treated with LPS after transfected with miR-25-3p mimic [50] miR-363 Downregulate IL-1β SH-SY5Y cells (human) under oxygen and glucose deprivation/reperfusion after transfected with miR-363-3p mimics [51] Coronary arterial endothelial cells (mouse) after transfected with miR-363-3p mimic and inhibitor [52] Downregulate IL-6 SH-SY5Y cells (human) under oxygen and glucose deprivation/reperfusion after transfected with miR-363-3p mimics [51] Coronary arterial endothelial cells (mouse) after transfected with miR-363-3p mimic and inhibitor [52] Downregulate TNFα SH-SY5Y cells (human) under oxygen and glucose deprivation/reperfusion after transfected with miR-363-3p mimics [51] Jurkat cells (human) after transfected with miR-363 mimic and inhibitor [53] miR To further investigate the pathophysiological backgrounds of the miRNA-based subgroups, we measured 387 proteins in plasma of the same patients (Figure 3A, and mean and SD values in Table S4). The protein profiles were available for 21 patients out of all the 26 patients due to the limited volume of the plasma samples.…”