MicroRNA-26b/PTEN Signaling Pathway Mediates Glycine-Induced Neuroprotection in SAH Injury

Qin, Xingping; Akter, Farhana; Qin, Lingxia; Xie, Qiurong; Liao, Xinyu; Li, Rui; Wu, Xia; Cheng, Nina; Shao, Lingmin; Xiong, Xiaoxing; Liu, Renzhong; Wan, Qi; Wu, Shi-Fang

doi:10.1007/s11064-019-02886-2

Cited by 17 publications

(15 citation statements)

References 39 publications

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“…Studies showed that PTEN was directly regulated by several miRNAs involved in proinflammatory cytokines production, such as miR-718 [39], miR-92a [40] and miR-26b [41]. HMGB1/PTEN/β-catenin signaling, as a novel pathway, plays an important role in sepsis-induced lung injury [16].…”

Section: Discussionmentioning

confidence: 99%

MiR-22-3p suppresses sepsis-induced acute kidney injury by targeting PTEN

Wang

Kong

et al. 2020

Bioscience Reports

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Background: Septic acute kidney injury is considered as a severe and frequent complication that occurs during sepsis. The present study was performed to understand the role of miR-22-3p and its underlying mechanism in sepsis-induced acute kidney injury. Methods: Rats were injected with adenovirus carrying miR-22-3p or miR-NC in the caudal vein before cecal ligation. Meanwhile, HK-2 cells were transfected with the above adenovirus following LPS stimulation. We measured the markers of renal injury (blood urea nitrogen (BUN), serum creatinine (SCR)). Histological changes in kidney tissues were examined by hematoxylin and eosin (H&E), Masson staining, periodic acid Schiff staining and TUNEL staining. The levels of IL-1β, IL-6, TNF-α and NO were determined by ELISA assay. Using TargetScan prediction and luciferase reporter assay, we predicted and validated the association between PTEN and miR-22-3p. Results: Our data showed that miR-22-3p was significantly down-regulated in a rat model of sepsis-induced acute kidney injury, in vivo and LPS-induced sepsis model in HK-2 cells, in vitro. Overexpression of miR-22-3p remarkably suppressed the inflammatory response and apoptosis via down-regulating HMGB1, p-p65, TLR4 and pro-inflammatory factors (IL-1β, IL-6, TNF-α and NO), both in vivo and in vitro. Moreover, PTEN was identified as a target of miR-22-3p. Furthermore, PTEN knockdown augmented, while overexpression reversed the suppressive role of miR-22-3p in LPS-induced inflammatory response. Conclusions: Our results showed that miR-22-3p induced protective role in sepsis-induced acute kidney injury may rely on the repression of PTEN.

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Section: Discussionmentioning

confidence: 99%

MiR-22-3p suppresses sepsis-induced acute kidney injury by targeting PTEN

Wang

Kong

et al. 2020

Bioscience Reports

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“…Pten/Akt signaling has been implicated in SAH pathogenesis. S473 Phosphorylation of Akt can protect neuron from death 47 , while the upstream regulator PTEN inhibited neuronal survival 28,48 . In this study, we demonstrated that PTEN was upregulated in OxyHb-treated neurons and prefrontal cortex of SAH-insulted rats and EVderived miR-21-5p from mesenchymal stem cells could significantly inhibited PTEN expression to protect neuronal apoptosis and improve cognitive function.…”

Section: Discussionmentioning

confidence: 99%

Extracellular vesicle-mediated transfer of miR-21-5p from mesenchymal stromal cells to neurons alleviates early brain injury to improve cognitive function via the PTEN/Akt pathway after subarachnoid hemorrhage

Gao

Xiong

et al. 2020

Cell Death Dis

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Patients with subarachnoid hemorrhage (SAH) often suffer from cognitive function impairments even when they have received proper treatment, such as the clipping or coiling of aneurysms, and this causes problems with returning to work and burdens the family. Increasing attention has been paid to mesenchymal stem cell (MSC)-derived extracellular vesicle (MSC-EV) as promising therapeutic vesicles for stroke management. In this study, we explored the potential role of MSC-EV in a rat model of SAH. We observed that MSC-EV ameliorated early brain injury (EBI) after SAH by reducing the apoptosis of neurons and that SAH induced an increase in the expression level of miR-21 in the prefrontal cortex and hippocampus. In addition, using miRNA profiling and CSF sequencing data from the exRNA Atlas, we demonstrated that EV-derived miR-21 protected neurons from apoptosis and alleviated SAH-induced cognitive dysfunction. The neuroprotective role of MSC-EV was abrogated by miR-21 knockdown or the administration of MK2206, a PTEN/Akt inhibitor. Overall, our results suggest that MSC-EV promotes neuronal survival and alleviates EBI after SAH through transferring miR-21 to recipient neurons.

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“…For example, miR-132 is upregulated in AD patients and promotes neuronal apoptosis by promoting Tau phosphorylation [31]. In the subarachnoid hemorrhage (SAH) model, glycine exerts neuroprotective effects through regulating the inflammatory response after SAH by regulating the miR-26b/PTEN signaling pathway [32]. In ischemic brain injury, miR-7a-5p can improve hypoxic-ischemic neuron damage by targeting α-synuclein (α-Syn), a protein that induces mitochondrial fragmentation, oxidative stress, and autophagy that promote neuronal cell death [33].…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine had neuroprotective effects on hippocampal neuronal cells via targeting lncRNA SHNG16 mediated microRNA-10b-5p/BDNF axis

et al. 2020

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Dexmedetomidine (DEX), a highly selective alpha2 adrenergic receptor agonist, is a commonly used anesthetic drug in surgical procedures. Previous studies have indicated that DEX exerts neuroprotective effects while the detailed mechanism has not been fully elucidated. Here, we aim to study the role of lncRNA SHNG16 in DEX-induced brain protection and its underlying molecular mechanism. The rats underwent middle cerebral artery occlusion (MCAO) surgery and oxygen-glucose deprivation (OGD)-treated HT22 hippocampal neurons were treated with DEX, respectively. CCK8 was used to evaluate cell viability. sh-SHNG16 as well as miR-10b-5p mimics were transfected into hippocampal neurons to further explore the bio-function of SNHG16 and miR-10b-5p in vitro. Furthermore, the interactions between SHNG16 and miR-10b-5p, miR-10b-5p and BDNF gene were confirmed by dual-luciferase report assay. Our data revealed that DEX attenuated neurological damage of the MCAO rats and also increased the cell viability of the neurons significantly. Besides, expression of SHNG16 and BDNF were both downregulated while miR-10b-5p was upregulated in MCAO brain tissues or OGD treated neurons. DEX inhibited miR-10b-5p expression but increased SHNG16 and BDNF levels with a dosage effect. After transfection with sh-SHNG16 or miR-10b-5p mimics, the expression of BDNF protein was downregulated, accompanied with decreased neuron viability. Dual-luciferase assay showed that SHNG16 targeted on miR-10b-5p, which also could bind directly to the 3′-UTR sites of BDNF and negatively regulate its expression. In conclusion, DEX exerts neuroprotective in ischemic stroke via improving neuron damage, the underlying mechanism may be upregulating SHNG16 and BDNF via sponging miR-10b-5p.

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MicroRNA-26b/PTEN Signaling Pathway Mediates Glycine-Induced Neuroprotection in SAH Injury

Cited by 17 publications

References 39 publications

MiR-22-3p suppresses sepsis-induced acute kidney injury by targeting PTEN

MiR-22-3p suppresses sepsis-induced acute kidney injury by targeting PTEN

Extracellular vesicle-mediated transfer of miR-21-5p from mesenchymal stromal cells to neurons alleviates early brain injury to improve cognitive function via the PTEN/Akt pathway after subarachnoid hemorrhage

Dexmedetomidine had neuroprotective effects on hippocampal neuronal cells via targeting lncRNA SHNG16 mediated microRNA-10b-5p/BDNF axis

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