<i>Retracted</i>: microRNA‐129‐5p involved in the neuroprotective effect of dexmedetomidine on hypoxic‐ischemic brain injury by targeting COL3A1 through the Wnt/β‐catenin signaling pathway in neonatal rats

Zhou, Xiumin; Liu, Jie; Wang, Ying; Zhang, Shuli; Zhao, Xin; Xu, Xiang Xi; Pei, Jian; Zhang, Man-He

doi:10.1002/jcb.26704

Cited by 15 publications

(16 citation statements)

References 44 publications

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“…Our team of researchers had previously found that miR-129-5p could exercise its protective effect of DEX on neonatal rats with HIBD by regulating the Wnt-catenin signaling pathway by targeting COL3A1. 11 According to the Miranda software, MEG3 could bind to miR-129-5p ( Figure 1A). The dual-luciferase reporter gene assay was utilized to verify the target relationship between MEG3 and miR-129-5p.…”

Section: Discussionmentioning

confidence: 99%

Silencing of long noncoding RNA MEG3 enhances cerebral protection of dexmedetomidine against hypoxic‐ischemic brain damage in neonatal mice by binding to miR‐129‐5p

Zhou

Liu

Wang

et al. 2018

J of Cellular Biochemistry

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Hypoxic‐ischemic brain damage (HIBD) is a leading cause of neonatal acute mortality and chronic nervous system injury. Recently, it has been found that long noncoding RNAs (lncRNAs) play a significant role in the neurodevelopment and etiopathogenesis of HIBD. Here, the researchers aimed to determine the role of lncRNA maternally expressed gene (MEG3) in the therapeutic effect of dexmedetomidine (DEX) in neonatal mice with HIBD through the regulation of microRNA‐129‐5p (miR‐129‐5p). HIBD models were established in C57/BL6 neonatal mice. Subsequently, the target relationship between MEG3 and miR‐129‐5p was predicted and verified. The neonatal mice were injected with DEX, ad‐shMEG3, and mimics and inhibitors of miR‐129‐5p to identify roles of MEG3 and miR‐129‐5p in therapeutic effects of DEX on neuronal apoptosis and injury, cerebral atrophy, and learning and memory ability of neonatal mice with HIBD. MEG3 directly targeted and inhibited the expression of miR‐129‐5p. Silencing of MEG3 or upregulation of miR‐129‐5p effectively promoted the therapeutic effect of DEX on neonatal mice with HIBD. Silencing of MEG3 or upregulation of miR‐129‐5p reduced the neuronal apoptosis rate and degree of cerebral atrophy, and also enhanced the learning and memory ability of HIBD neonatal mice. Collectively, the key findings obtained from the present study support the notion that MEG3 silencing enhances the therapeutic effect of DEX on neonatal mice with HIBD by binding to miR‐129‐5p.

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Section: Discussionmentioning

confidence: 99%

Silencing of long noncoding RNA MEG3 enhances cerebral protection of dexmedetomidine against hypoxic‐ischemic brain damage in neonatal mice by binding to miR‐129‐5p

Zhou

Liu

Wang

et al. 2018

J of Cellular Biochemistry

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“…Mir-138 affects the formation of fear memory by modifying the expression of the downstream target gene calpain 1 (Capn1) with major implications on the synaptic plasticity. Recently mir-129 has also been associated with memory retention, in addition to its neuroprotective role on hypoxic-ischaemic brain injuries [39]. As shown by Fernandez et al [40] mir-129 and mir-144 play a major role in the modulation of the hippocampal microRNA-mRNA regulatory network upon physical exercise, which eventually lead to improvements in memory detention.…”

Section: Function-and Tissue-specific Expression Of Mirnamentioning

confidence: 96%

Deep sequencing of small non-coding RNA highlights brain-specific expression patterns and RNA cleavage

et al. 2019

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With the advance of high-throughput sequencing technology numerous new regulatory small RNAs have been identified, that broaden the variety of processing mechanisms and functions of non-coding RNA. Here we explore small non-coding RNA (sncRNA) expression in central parts of the physiological stress and anxiety response system. Therefore, we characterize the sncRNA profile of tissue samples from Amygdala, Hippocampus, Hypothalamus and Adrenal Gland, obtained from 20 pigs. Our analysis reveals that all tissues but Amygdala and Hippocampus possess distinct, tissue-specific expression pattern of miRNA that are associated with Hypoxia, stress responses as well as memory and fear conditioning. In particular, we observe marked differences in the expression profile of limbic tissues compared to those associated to the HPA/stress axis, with a surprisingly high aggregation of 3´-tRNA halves in Amygdala and Hippocampus. Since regulation of sncRNA and RNA cleavage plays a pivotal role in the central nervous system, our work provides seminal insights in the role/involvement of sncRNA in the transcriptional and post-transcriptional regulation of negative emotion, stress and coping behaviour in pigs, and mammals in general.

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“…Previous studies have reported the interaction between DEX and miRNAs in neuroprotection against ischemic hypoxia injury, for examples, Han et al (2018) showed clearly that miR-140-5p enhanced the cerebral protective effects of DEX against HIBD in neonatal rats by directly binding to WNT1 through the negative regulation of the Wnt/β-catenin signal pathway (Han et al, 2018); Wang et al (2019) noticed that DEX could carry out its neuroprotective effects though modulating the relationship between miR2233p and TIAL1; Zhou et al (2018) suggest that miR-129-5p was able to improve neuroprotective role of DEX in HIBI by targeting COL3A1 via Wnt/β-catenin signaling pathway in neonatal rats (Fan et al, 2020). To determine whether miR-206 was implicated in neuroprotection of DEX, we detected the expression of miR-206 in H 2 O 2 and/or DEX treated SK-N-SH cells.…”

Section: Discussionmentioning

confidence: 99%

MiR-206 is involved in neuroprotective effects of Dexmedetomidine in H2O2-induced SK-N-SH cells by targeting ANXA1

et al. 2022

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This study focused on exploring the neuroprotective role of Dexmedetomidine (DEX) and miR-206 in H 2 O 2 -induced SK-N-SH cells. First, we dectected the cell viability, apotosis, oxidative stress and miR-206 expression in H 2 O 2 -treated SK-N-SH cells. Next, we examined above content in H 2 O 2 -induced SK-N-SH cells though DEX treatment. Besides, the level of cell viability, apotosis, oxidative stress were evaluated in H 2 O 2 -treated SK-N-SH cells transfected with miR-206 mimics and miR-206 inhibitor. Moreover, the target gene of miR-206 were predicted and verifed by binformatics tools and luciferase reporter assay. These data indicated that H 2 O 2 evoked the apotosis, oxidative stress and inhibition of miR-206 expression in SK-N-SH cells in a dose manner. Besides, DEX attenuated H 2 O 2 -induced oxidative damage, apotosis and promoted miR-206 expression in SK-N-SH cells. Moreover, overexpression of miR-206 augmented the cell viablity as well as suppressed apotosis and oxidative stress in H 2 O 2 -induced SK-N-SH cells, while down-expression of miR-206 showed opppsite effects. Further, Annexin A1 (ANXA1) was verified as a directly target of miR-206, and over-expression of ANXA1 could slack the neuroprotective effect of miR-206 in H 2 O 2 -induced SK-N-SH cells. DEX exerted neuroprotective effects on H 2 O 2 -treated SK-N-SH cells in vitro by negatively reguating ANXA1 expression via activation of miR-206.

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Retracted: microRNA‐129‐5p involved in the neuroprotective effect of dexmedetomidine on hypoxic‐ischemic brain injury by targeting COL3A1 through the Wnt/β‐catenin signaling pathway in neonatal rats

Cited by 15 publications

References 44 publications

Silencing of long noncoding RNA MEG3 enhances cerebral protection of dexmedetomidine against hypoxic‐ischemic brain damage in neonatal mice by binding to miR‐129‐5p

Silencing of long noncoding RNA MEG3 enhances cerebral protection of dexmedetomidine against hypoxic‐ischemic brain damage in neonatal mice by binding to miR‐129‐5p

Deep sequencing of small non-coding RNA highlights brain-specific expression patterns and RNA cleavage

MiR-206 is involved in neuroprotective effects of Dexmedetomidine in H2O2-induced SK-N-SH cells by targeting ANXA1

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