miR-211-5p alleviates focal cerebral ischemia-reperfusion injury in rats by down-regulating the expression of COX2

Peng, Zhe; Li, Miaomiao; Tan, Xiaodan; Xiang, Ping; Wang, Hong; Luo, Ying; Yang, Yang; Huang, Haifeng; Chen, Zhihao; Xia, Hui; Li, Yuke; Zhang, Jiahua; Gu, Chao; Liu, Maozhu; Wang, Qiong; Yang, Junqing

doi:10.1016/j.bcp.2020.113983

Cited by 40 publications

(19 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Through using starBase software, we predicted the candidate miRNA targets of GAS5. Among all these predicted targets, six miRNAs were screened out due to their vital roles in regulating cerebral ischemia-reperfusion injury, including miR-34b-3p, 13 miR-485-3p, 16 miR-211-5p, 17 miR-217-5p, 18 miR-874-3p 19 and miR-338-5p. 20 We tested the regulatory relationships between GAS5 and these candidate targets.…”

Section: Resultsmentioning

confidence: 99%

LncRNA GAS5 Silencing Attenuates Oxygen-Glucose Deprivation/Reperfusion-Induced Injury in Brain Microvascular Endothelial Cells via miR-34b-3p-Dependent Regulation of EPHA4

Shen¹,

Wang²,

Xu³

et al. 2021

NDT

View full text Add to dashboard Cite

Background:The aim of our study was to explore the role of long non-coding RNA (lncRNA) growth arrest-specific 5 (GAS5) in ischemic stroke using oxygen-glucose deprivation/reperfusion (OGD/R)-induced bEnd.3 cells as in vitro cell model. Methods: Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot assay were adopted to analyze RNA and protein expression. Cell viability and apoptosis were analyzed by Cell Counting Kit-8 (CCK8) assay and flow cytometry. The levels of nitric oxide (NO) and endothelin-1 (ET-1) in culture supernatant were examined by their matching commercial kits. The intermolecular target interaction was predicted by starBase software and tested by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Results: OGD/R-induced apoptosis and dysregulation in vascular endocrine system were largely alleviated by the knockdown of GAS5. GAS5 interacted with microRNA-34b-3p (miR-34b-3p), and GAS5 silencing protected bEnd.3 cells from OGD/R-induced injury partly through up-regulating miR-34b-3p. EPH receptor A4 (EPHA4) was a target of miR-34b-3p. GAS5 acted as the molecular sponge of miR-34b-3p to up-regulate EPHA4 in bEnd.3 cells. GAS5 interference protected against OGD/R-induced damage in bEnd.3 cells partly through down-regulating EPHA4. Conclusion: LncRNA GAS5 knockdown protected brain microvascular endothelial cells bEnd.3 from OGD/R-induced injury depending on the regulation of miR-34b-3p/EPHA4 axis.

show abstract

Section: Resultsmentioning

confidence: 99%

LncRNA GAS5 Silencing Attenuates Oxygen-Glucose Deprivation/Reperfusion-Induced Injury in Brain Microvascular Endothelial Cells via miR-34b-3p-Dependent Regulation of EPHA4

Shen¹,

Wang²,

Xu³

et al. 2021

NDT

View full text Add to dashboard Cite

show abstract

“…miR-211 has reported to reduce neuron apoptosis in a neonatal rat model of hypoxic-ischemic injury [ 41 ], and alleviates focal cerebral ischemia-reperfusion injury in rats [ 25 , 42 ]. In this study, we found that miR-211 was downexpressed both in proximal renal tubular cells subjected to H/R and in mice kidney subjected to I/R injury.…”

Section: Discussionmentioning

confidence: 99%

miR-211 alleviates ischaemia/reperfusion-induced kidney injury by targeting TGFβR2/TGF-β/SMAD3 pathway

et al. 2020

View full text Add to dashboard Cite

MicroRNA-211 (miR-211) is closely related to apoptosis and plays an important role in ischemia/reperfusion (I/R) injury. Whether miR-211 is involved in the protective effects in renal I/R injury is unknown. In this study, we evaluated the role of miR-211 in human tubular epithelial cells in response to hypoxia-reoxygenation (H/R) stimulation and I/R injury in vitro and in vivo . The results revealed that miR-211 was down-regulated and TGFβR2 was up-regulated in human kidney (HK-2) cells subjected to H/R. Luciferase reporter assay showed that TGFβR2 was a direct target of miR-211. Enforced miR-211 expression decreased H/R-induced HK-2 cell apoptosis and increased cell viability, and targeting miR-211 further increased H/R-induced HK-2 cell apoptosis and decreased cell viability. However, the effect of miR-211 was reversed by targeting TGFβR2 or enforced TGFβR2 expression in miR-211 overexpressing cells or miR-211 downexpressing cells. Moreover, we confirmed that miR-211 interacted with TGFβR2, and regulating TGF-β/SMAD3 signal. In vivo in mice, miR-211 overexpression ameliorates biochemical and histological kidney injury, reduces apoptosis in mice following I/R. On the contrary, miR-211 downexpressing promoted histological kidney injury and increased apoptosis in mice following I/R. Inhibition of miR-211 or miR-211 overexpression inhibited TGF-β/SMAD3 pathways or activated TGF-β/SMAD3 signal pathways in vitro and in vivo , which are critical for cell survival. Our findings suggested that miR-211 suppress apoptosis and relieve kidney injury following H/R or I/R via targeting TGFβR2/TGF-β/SMAD3 signals. Therefore, miR-211 may be as therapeutic potential for I/R- induced kidney injury.

show abstract

“…It is found that, under the ischemia-reperfusion injury, the level of COX-2 is increased. Inhibition of COX-2 expression can reduce the production of inflammatory factors and alleviate the ischemia-reperfusion injury 5 .…”

Section: Introductionmentioning

confidence: 99%

Parecoxib mitigates lung ischemia-reperfusion injury in rats by reducing oxidative stress and inflammation and up-regulating HO-1 expression

Qin

Jin

et al. 2021

Acta Cir. Bras.

View full text Add to dashboard Cite

Purpose: To investigate the protective effect of parecoxib against lung ischemia-reperfusion injury (LIRI) in rats and the mechanism. Methods: Thirty rats were divided into sham-operated, LIRI and LIRI+parecoxib groups. LIRI model (ischemia for 60 min, followed by reperfusion for 120 min) was constructed in LIRI and LIRI+parecoxib groups. In LIRI+parecoxib group, 10 mg/kg parecoxib was given via femoral vein 15 min before ischemia beginning. At the end of the reperfusion, blood gas analysis, lung wet to dry mass ratio measurement, lung tissue biochemical determination and heme oxygenase-1 (HO-1) protein expression determination were performed. Results: Compared with LIRI group, in LIRI+parecoxib group the oxygenation index was significantly increased, the alveolar-arterial oxygen partial pressure difference was significantly decreased, the lung wet to dry mass ratio was significantly decreased, the lung tissue malondialdehyde content was significantly decreased, the lung tissue superoxide dismutase and myeloperoxidase activities were significantly increased, the lung tissue tumor necrosis factor α and interleukin 1β levels were significantly decreased, and the lung tissue HO-1 protein expression level was significantly increased (all P < 0.05). Conclusion: Parecoxib pretreatment can mitigate the LIRI in rats by reducing oxidative stress, inhibiting inflammatory response and upregulating HO-1 expression in lung tissue.

show abstract

miR-211-5p alleviates focal cerebral ischemia-reperfusion injury in rats by down-regulating the expression of COX2

Cited by 40 publications

References 51 publications

LncRNA GAS5 Silencing Attenuates Oxygen-Glucose Deprivation/Reperfusion-Induced Injury in Brain Microvascular Endothelial Cells via miR-34b-3p-Dependent Regulation of EPHA4

LncRNA GAS5 Silencing Attenuates Oxygen-Glucose Deprivation/Reperfusion-Induced Injury in Brain Microvascular Endothelial Cells via miR-34b-3p-Dependent Regulation of EPHA4

miR-211 alleviates ischaemia/reperfusion-induced kidney injury by targeting TGFβR2/TGF-β/SMAD3 pathway

Parecoxib mitigates lung ischemia-reperfusion injury in rats by reducing oxidative stress and inflammation and up-regulating HO-1 expression

Contact Info

Product

Resources

About