Inhibition of microRNA-429 attenuates oxygen–glucose deprivation/reoxygenation-induced neuronal injury by promoting expression of GATA-binding protein 4

Xiao, Jie; Kong, Ranran; Hu, Jingye

doi:10.1097/wnr.0000000000001023

Cited by 10 publications

(8 citation statements)

References 24 publications

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“…their study that inhibited miR-429 could attenuate oxygen-glucose deprivation/reoxygenation-induced neuronal injury through GATA-binding protein 4 [24]. We have also found in this study that restrained miR-429 could relieve the inflammation in CHD by repressing the expression of inflammation-related factors IL-1β, IL-6, and TNF-α.…”

Section: Discussionsupporting

confidence: 74%

RETRACTED ARTICLE: Down-regulation of microRNA-429 alleviates myocardial injury of rats with coronary heart disease

Yang

Zhang

et al. 2019

Cell Cycle

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In recent years, the impact of microRNAs (miRNAs) on coronary heart disease (CHD) has been identified. This study was aimed to investigate the regulative role of microRNA (miR-429) in myocardial injury of rats with CHD. Expression of miR-429 in CHD patients and healthy people was detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR). The CHD rat models were injected with normal saline, mimics negative control (NC), miR-429 mimics, inhibitors NC and miR-429 inhibitors twice a week, for 4 weeks. Levels of inflammatory factors, oxidative stress indices as well as apoptosis of cardiomyocytes were determined by a series of assays. Expression of miR-429 was up-regulated in CHD patients. Reduced miR-429 could decline the expression of oxidative stress-related factors and inflammation-related factors, and inhibit the apoptosis of cardiomyocytes in rats with CHD. Moreover, the down-regulation of miR-429 could promote the expression of CrkL and repress activation of the MEK/ERK signaling pathway. This study reveals that restrained miR-429 could exert a protective impact on myocardial injury of rats with CHD by suppressing oxidative stress, inflammation reaction and apoptosis of cardiomyocytes. The function mechanisms may relate to the up-regulation of CrkL and inhibition of the MEK/ERK signaling pathway.

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Section: Discussionsupporting

confidence: 74%

RETRACTED ARTICLE: Down-regulation of microRNA-429 alleviates myocardial injury of rats with coronary heart disease

Yang

Zhang

et al. 2019

Cell Cycle

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“…GATA4 has been identified as an antiapoptotic protein that protects cardiomyocytes against hypoxia, IRI, and doxorubicin-induced apoptosis ( Kobayashi et al, 2006 ). A study has shown that GATA4 was reduced by OGD/R-induced neuronal apoptosis, indicating a neuroprotective function of GATA4 ( Xiao, Kong & Hu, 2018 ). RBPJ is a key transcription factor downstream of receptor activation in the canonical Notch signaling pathway ( Zheng et al, 2009 ).…”

Section: Discussionmentioning

confidence: 99%

Identification of key microRNAs and the underlying molecular mechanism in spinal cord ischemia-reperfusion injury in rats

Chen

Han

Wang

2021

PeerJ

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Spinal cord ischemia-reperfusion injury (SCII) is a pathological process with severe complications such as paraplegia and paralysis. Aberrant miRNA expression is involved in the development of SCII. Differences in the experimenters, filtering conditions, control selection, and sequencing platform may lead to different miRNA expression results. This study systematically analyzes the available SCII miRNA expression data to explore the key differently expressed miRNAs (DEmiRNAs) and the underlying molecular mechanism in SCII. A systematic bioinformatics analysis was performed on 23 representative rat SCII miRNA datasets from PubMed. The target genes of key DEmiRNAs were predicted on miRDB. The DAVID and TFactS databases were utilized for functional enrichment and transcription factor binding analyses. In this study, 19 key DEmiRNAs involved in SCII were identified, 9 of which were upregulated (miR-144-3p, miR-3568, miR-204, miR-30c, miR-34c-3p, miR-155-3p, miR-200b, miR-463, and miR-760-5p) and 10 downregulated (miR-28-5p, miR-21-5p, miR-702-3p, miR-291a-3p, miR-199a-3p, miR-352, miR-743b-3p, miR-125b-2-3p, miR-129-1-3p, and miR-136). KEGG enrichment analysis on the target genes of the upregulated DEmiRNAs revealed that the involved pathways were mainly the cGMP-PKG and cAMP signaling pathways. KEGG enrichment analysis on the target genes of the downregulated DEmiRNAs revealed that the involved pathways were mainly the Chemokine and MAPK signaling pathways. GO enrichment analysis indicated that the target genes of the upregulated DEmiRNAs were markedly enriched in biological processes such as brain development and the positive regulation of transcription from RNA polymerase II promoter. Target genes of the downregulated DEmiRNAs were mainly enriched in biological processes such as intracellular signal transduction and negative regulation of cell proliferation. According to the transcription factor analysis, the four transcription factors, including SP1, GLI1, GLI2, and FOXO3, had important regulatory effects on the target genes of the key DEmiRNAs. Among the upregulated DEmiRNAs, miR-3568 was especially interesting. While SCII causes severe neurological deficits of lower extremities, the anti-miRNA oligonucleotides (AMOs) of miR-3568 improve neurological function. Cleaved caspase-3 and Bax was markedly upregulated in SCII comparing to the sham group, and miR-3568 AMO reduced the upregulation. Bcl-2 expression levels showed a opposite trend as cleaved caspase-3. The expression of GATA6, GATA4, and RBPJ decreased after SCII and miR-3568 AMO attenuated this upregulation. In conclusion, 19 significant DEmiRNAs in the pathogenesis of SCII were identified, and the underlying molecular mechanisms were validated. The DEmiRNAs could serve as potential intervention targets for SCII. Moreover, inhibition of miR-3568 preserved hind limb function after SCII by reducing apoptosis, possibly through regulating GATA6, GATA4, and RBPJ in SCII.

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“…It's worth mentioning that EAA plays an important role in maintaining the homeostasis of the central nervous system, over-expression of NMDAR is the key step leading to excitotoxicity, this excitotoxic effect is also the key to the death of neurons in the pathological state of ischemic brain injury. 26,27) As previously reported, the excessive accumulation of extracellular glutamate will over-stimulates their receptor ion channels on postsynaptic and extrasynaptic neurons. 28) However, the cellular consequences of synaptic versus extrasynaptic NMDA receptor stimulation are dramatically different.…”

Section: Discussionmentioning

confidence: 81%

YiQi Tongluo Granule against Cerebral Ischemia/Reperfusion Injury in Rats by Freezing GluN2B and CaMK II through NMDAR/ERK1/2 Signaling

Li²,

Wang

et al. 2019

CHEMICAL & PHARMACEUTICAL BULLETIN

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Yiqi Tongluo Granule (YQTL) is a kind of proprietary Chinese medicine, manufactured by ChinaShineway Pharmaceutical Group Ltd., under the authority of China Food and Drug Administration (CFDA) treating cardiovascular and cerebrovascular diseases such as ischemic stroke in China, however the underlying mechanism of YQTL on treating ischemic stroke has not been revealed. This study is aimed to evaluate the protective effect of YQTL on cerebral ischemia/reperfusion (I/R) injury and inquire into its underlying mechanisms. Cerebral I/R injury was induced by occluding the middle cerebral artery for 2 h followed by 24 h reperfusion. And regional cerebral flow was monitored by Laser Doppler flow during ischemia phase. The infarct volume was evaluated by Triphenyte-trazolium chloride staining. The protective effects of YQTL were assessed by a number of parameters, including neurological scores, regional cerebral blood flow, pathological changes of neuron in hippocampuses and hippocampus calcium level. The proteins of extracellular signal-regulated kinase (ERK), N-methyl D-aspartate receptor subtype 2B (GluN2B) and p-calcium-dependent protein kinaseII (CaMKII) response were assayed by Western blotting. I/R caused significant change in neurological deficit scores, regional cerebral flow and infarct volume. However results in YQTL groups and Nimodipine Tablets (NMDP) group were reversed. Subsequently YQTL reduced I/R-induced calcium influx. Results of hematoxylin-eosin staining manifested that YQTL significantly improved neuronal injury after I/R in rats. Meanwhile, microdialysis data demonstrated that extracellular glutamate was increased in the striatum during ischemia reperfusion, which was reduced by YQTL. YQTL and mitogen-activated protein extracellular kinase (MEK) inhibitor suppressed the I/R-mediated over-expression of GluN2B, p-ERK, ERK and p-CaMKII proteins expression. Putting these together, our results suggest that YQTL played a neuroprotective role in cerebral I/R injury, which might be exerted by inhibiting the excitotoxicity and expression of GluN2B, p-CaMKII and MEK/ERK signal pathway.

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Inhibition of microRNA-429 attenuates oxygen–glucose deprivation/reoxygenation-induced neuronal injury by promoting expression of GATA-binding protein 4

Cited by 10 publications

References 24 publications

RETRACTED ARTICLE: Down-regulation of microRNA-429 alleviates myocardial injury of rats with coronary heart disease

RETRACTED ARTICLE: Down-regulation of microRNA-429 alleviates myocardial injury of rats with coronary heart disease

Identification of key microRNAs and the underlying molecular mechanism in spinal cord ischemia-reperfusion injury in rats

YiQi Tongluo Granule against Cerebral Ischemia/Reperfusion Injury in Rats by Freezing GluN2B and CaMK II through NMDAR/ERK1/2 Signaling

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