Dexmedetomidine protects PC12 cells from oxidative damage through regulation of miR-199a/HIF-1α

Wu, Ling; Yang, Xi; Kong, Qing

doi:10.1080/21691401.2020.1716780

Cited by 12 publications

(12 citation statements)

References 45 publications

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“…Wu et al confirmed that miR-49 inhibits angiogenesis in breast cancer by targeting HIF-1α (40). Previous studies confirmed that miR-199a protects PC12 cells from oxidative damage by regulating HIF-1α (17). In this study, it was found that downregulation of miR-199a expression could upregulate the expression of HIF-1α, and DMED could upregulate the expression of HIF-1α.…”

Section: Discussionsupporting

confidence: 61%

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Dexmetomidine promotes the activity of breast cancer cells through miR-199a/HIF-1α axis

Wen¹,

Xin²

2021

Transl Cancer Res TCR

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Background Breast cancer, as one of the most common malignant tumors in women, is still a great threat to women all over the world. Dexmetomidine (DMED) is a highly selective α2-adrenergic receptor agonist, which has attracted much attention in recent years. This study aimed to clarify the potential mechanism of DMED in regulating the activity of breast cancer cells. Methods Breast cancer cell lines MCF-7 and MDA-MB-231 were treated with DMED. The levels of miR-199a and HIF-1α mRNA were detected using quantitative real-time polymerase chain reaction (QRT-PCR); the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) and transwell assays were applied to monitor the activity of breast cancer cells; the apoptosis of breast cancer cells was detected using the caspase-3 activity assay and flow cytometry; binding of miR-199a and HIF-1α was assessed using double luciferase reporter gene assay, and western blot was employed to monitor the level of HIF-1α in cells. Results The cytotoxicity and apoptosis of MCF-7 and MDA-MB-231 cells was inhibited by DMED. It also downregulated the expression of miR-199a in breast cancer cells and enhanced the downregulation of miR-199a to promote the activity of breast cancer cells and inhibit apoptosis. Also, miR-199a targeted HIF-1α. Further functional experiments confirmed that DMED promoted the progression of breast cancer through the miR-199a/HIF-1α axis. Conclusions DMED promotes the activity of breast cancer cells through miR-199a/HIF-1αaxis. This can provide some reference for DMED in the clinical treatment of breast cancer.

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Section: Discussionsupporting

confidence: 61%

“…Also, MiR-199a has been shown to inhibit the activity of breast cancer cells (16). Wu et al have confirmed that DMED prevents oxidative damage to PC12 cells by regulating miR-199a/HIF-1α (17). At the same time, DMED attenuates neuronal injury induced by cerebral ischemia-reperfusion (IR) by regulating miR-199a (18).…”

Section: Introductionmentioning

confidence: 99%

Dexmetomidine promotes the activity of breast cancer cells through miR-199a/HIF-1α axis

Wen¹,

Xin²

2021

Transl Cancer Res TCR

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“…The present study found that DEX decreased mNSS and improved pathological damage of the cerebral cortex. A previous study also found that DEX protects PC12 cells from oxidative damage via regulation of miR-199a/hypoxia inducible factor 1α (36). Thus, the present study aimed to investigate the association between DEX and miR-199a in neuron injury.…”

Section: Discussionmentioning

confidence: 88%

Dexmedetomidine attenuates neuronal injury induced by cerebral ischemia‑reperfusion by regulating miR‑199a

Zhu

Zhao

Zhang³

et al. 2021

Mol Med Rep

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As is well known, dexmedetomidine (DEX) serves a neuroprotective role in cerebral ischemia-reperfusion (CIR) injury, and microRNA (miR)-199a has been re-ported to be associated with IR injury. However, the association between DEX and miR-199a in CIR injury remains unknown. Thus, the aim of the present study was to verify whether the neuroprotective effect of DEX on cerebral ischemia-reperfusion rats is associated with miR-199a. A rat model of CIR was established, and the modified neurological severity score (mNSS) was evaluated. The effect of DEX on the patholog-ical structure of the cerebral cortex in CIR rats was observed by hematoxylin and eosin and Nissl staining. Reverse transcription-quantitative PCR was used to analyze the expression levels of miR-199a in brain tissue following intracerebroventricular injection of miR-199a antagomir. The co-expression of NeuN and microtubule-associated proteins 1A/1B light chain 3B in the cerebral cortex was analyzed by immunofluorescence staining. Western blotting and immunohistochemistry were performed to analyze the expression of autophagy-associated proteins in the brain tissue. DEX inhibited the expression of miR-199a, decreased the mNSS and improved pathological damage to the cerebral cortex. DEX also inhibited autophagy and expression levels of associated proteins and decreased nerve cell injury. In conclusion, DEX inhibited expression of miR-199a and improved neurocyte injury induced by CIR.

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“…The miR-199 regulates cell proliferation, apoptosis, and ROS production by affecting the Wnt/b-catenin, PI3K/AKT/mTOR, and HIF-1α signalling pathways. In PC 12 cells with H 2 O 2 -induced oxidative injury, dexmedetomidine reduced ROS formation and apoptosis by regulating miR-199a/HIF-1 and simulating PI3K/AKT/mTOR and Wnt/b-catenin signalling pathways (Wu et al, 2020).…”

Section: Neuroprotective Effect Of Dexmedetomidine In Substance-induced Neuronal Injurymentioning

confidence: 93%

The potential role of dexmedetomidine on neuroprotection and its possible mechanisms: Evidence from in vitro and in vivo studies

Unchiti

Leurcharusmee

Samerchua

et al. 2021

Eur J of Neuroscience

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Neurological disorders following brain injuries and neurodegeneration are on the rise worldwide and cause disability and suffering in patients. It is crucial to explore novel neuroprotectants. Dexmedetomidine, a selective α2-adrenoceptor agonist, is commonly used for anxiolysis, sedation and analgesia in clinical anaesthesia and critical care. Recent studies have shown that dexmedetomidine exerts protective effects on multiple organs. This review summarized and discussed the current neuroprotective effects of dexmedetomidine, as well as the underlying mechanisms. In preclinical studies, dexmedetomidine reduced neuronal injury and improved functional outcomes in several models, including hypoxia-induced neuronal injury, ischaemic-reperfusion injury, intracerebral haemorrhage, post-traumatic brain injury, anaesthetic-induced neuronal injury, substance-induced neuronal injury, neuroinflammation, epilepsy and neurodegeneration. Several mechanisms are associated with the neuroprotective function of dexmedetomidine, including neurotransmitter regulation, inflammatory response, oxidative stress, apoptotic pathway, autophagy, mitochondrial function and other cell signalling pathways. In summary, dexmedetomidine has the potential to be a novel neuroprotective agent for a wide range of neurological disorders.

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Dexmedetomidine protects PC12 cells from oxidative damage through regulation of miR-199a/HIF-1α

Cited by 12 publications

References 45 publications

Dexmetomidine promotes the activity of breast cancer cells through miR-199a/HIF-1α axis

Dexmetomidine promotes the activity of breast cancer cells through miR-199a/HIF-1α axis

Dexmedetomidine attenuates neuronal injury induced by cerebral ischemia‑reperfusion by regulating miR‑199a

The potential role of dexmedetomidine on neuroprotection and its possible mechanisms: Evidence from in vitro and in vivo studies

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