MicroRNA-29b alleviates oxygen and glucose deprivation/reperfusion-induced injury via inhibition of the p53‑dependent apoptosis pathway in N2a neuroblastoma cells

Cao, Lei; Zhang, Shuai; Jiang, Tianyan; Chen, Li; Liu, Jing; Zhou, Shi

doi:10.3892/etm.2017.5410

Cited by 19 publications

(15 citation statements)

References 45 publications

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“…For example, Zhu et al () constructed the OGD model and probed the protective impacts of ginsenoside Rb3 on OGD‐evoked PC‐12 cell ischemic injury. Cao et al () confirmed the protective impacts of miR‐29b on OGD/R‐evoked cell injury in N2a neuroblastoma cells. Wang et al () discovered that the repression of miR‐142‐5p could alleviate OGD/R‐evoked neuron injury via mediating Nrf2/ARE signaling pathway.…”

Section: Discussionmentioning

confidence: 83%

Retracted: MicroRNA‐132 protects H9c2 cells against oxygen and glucose deprivation‐evoked injury by targeting FOXO3A

Zhang

Gong

et al. 2019

Journal Cellular Physiology

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Myocardial ischemia/reperfusion injury (MIRI) is a clinically familiar disease, which possesses a great negative impact on human health. But, the effective treatment is still absent. MicroRNAs (miRNAs) have been testified to play a momentous role in MIRI. The purpose of the study aimed to probe the functions of miR-132 in oxygen and glucose deprivation (OGD)-evoked injury in H9c2 cells. miR-132 expression in H9c2 cells accompanied by OGD disposition was evaluated via real-time quantitative polymerase chain reaction. After miR-132 mimic and inhibitor transfections, the impacts of miR-132 on OGD-affected H9c2 cell viability, apoptosis, cell cycle, and the interrelated factors were appraised by exploiting cell counting kit-8, flow cytometry, and western blot analysis. FOXO3A expression was estimated in above-transfected cells, meanwhile, the correlation between miR-132 and FOXO3A was probed by dualluciferase report assay. Ultimately, above mentioned cell processes were reassessed in H9c2 cells after preprocessing OGD administration and transfection with si-FOXO3A and si-NC plasmids. We got that OGD disposition obviously enhanced miR-132 expression in H9c2 cells. Overexpressed miR-132 evidently reversed OGDevoked cell viability repression and apoptosis induction in H9c2 cells. In addition, overexpressed miR-132 mitigated OGD-evoked G0/G1 cell arrest by mediating p21, p27, and cyclin D1 expression. Repression of FOXO3A was observed in miR-132mimic-transfected cells, which was also predicated as a direct gene of miR-132. We discovered that silenced FOXO3A alleviated OGD-evoked cell injury in H9c2 cells via facilitating cell viability, hindering apoptosis and restraining cell arrest at G0/G1 phase. In conclusion, these investigations corroborated that miR-132 exhibited the protective impacts on H9c2 cells against OGD-evoked injury via targeting FOXO3A.

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Section: Discussionmentioning

confidence: 83%

Retracted: MicroRNA‐132 protects H9c2 cells against oxygen and glucose deprivation‐evoked injury by targeting FOXO3A

Zhang

Gong

et al. 2019

Journal Cellular Physiology

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“…Furthermore, in vivo and in vitro knock down models of miR-29b demonstrated loss of neuronal viability in spinal cord injury or dorsal root ganglia [76,126], while delivery of a miR-29b-3p -mimic, prohibits chemotherapeutically induced apoptosis in cardiomyocytes through regulation of the mitochondria-dependent apoptotic pathway [117]. The overexpression of miR-29b-3p could alleviate or prevent OGD-induced (oxygen-glucose deprivation) damage [132,133], whereas its loss led to aggravation of the situation [134]. As shown in optic nerves of zebra fish, raised miR-29b-3p level is believed to play a key role in central nerve regeneration by directly aiming filaments of the cytoskeleton [135].…”

Section: Discussionmentioning

confidence: 99%

Deregulated miR-29b-3p Correlates with Tissue-Specific Activation of Intrinsic Apoptosis in An Animal Model of Amyotrophic Lateral Sclerosis

Klatt

Theis

Hahn

et al. 2019

Cells

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Amyotrophic lateral sclerosis (ALS) is one of the most common incurable motor neuron disorders in adults. The majority of all ALS cases occur sporadically (sALS). Symptoms of ALS are caused by a progressive degeneration of motor neurons located in the motor cortex and spinal cord. The question arises why motor neurons selectively degenerate in ALS, while other cells and systems appear to be spared the disease. Members of the intrinsic apoptotic pathway are frequent targets of altered microRNA expression. Therefore, microRNAs and their effects on cell survival are subject of controversial debates. In this study, we investigated the expression of numerous members of the intrinsic apoptotic cascade by qPCR, western blot, and immunostaining in two different regions of the CNS of wobbler mice. Further we addressed the expression of miR-29b-3p targeting BMF, Bax, and, Bak, members of the apoptotic pathway. We show a tissue-specific differential expression of BMF, Bax, and cleaved-Caspase 3 in wobbler mice. An opposing regulation of miR-29b-3p expression in the cerebellum and cervical spinal cord of wobbler mice suggests different mechanisms regulating the intrinsic apoptotic pathway. Based on our findings, it could be speculated that miR-29b-3p might regulate antiapoptotic survival mechanisms in CNS areas that are not affected by neurodegeneration in the wobbler mouse ALS model.

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“…However, this therapy inevitably leads to ischaemia/reperfusion injury (IRI) and its treatment effect is limited. Accumulating evidence shows that apoptosis and death of nerve cells after I/R are the main causes of aggravating brain injury . Therefore, it is important to develop novel therapeutic strategies to treat cerebral IRI.…”

Section: Introductionmentioning

confidence: 99%

“…Accumulating evidence shows that apoptosis and death of nerve cells after I/R are the main causes of aggravating brain injury. 4,5 Therefore, it is important to develop novel therapeutic strategies to treat cerebral IRI.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA TUG1 contributes to cerebral ischaemia/reperfusion injury by sponging mir‐145 to up‐regulate AQP4 expression

Shan

Chen

Zhao

et al. 2019

J Cellular Molecular Medi

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Emerging studies have shown that long noncoding RNA (lncRNA) TUG1 (taurine‐up‐regulated gene 1) plays critical roles in multiple biological processes. However, the expression and function of lncRNA TUG1 in cerebral ischaemia/reperfusion injury have not been reported yet. In this study, we found that LncRNA TUG1 expression was significantly up‐regulated in cultured MA‐C cells exposed to OGD/R injury, while similar results were also observed in MCAO model. Mechanistically, knockdown of TUG1 decreased lactate dehydrogenase levels and the ratio of apoptotic cells and promoted cell survival in vitro. Moreover, knockdown of TUG1 decreased AQP4 (encoding aquaporin 4) expression to attenuate OGD/R injury. TUG1 could interact directly with miR‐145, and down‐regulation of miR‐145 could efficiently reverse the function of TUG1 siRNA on AQP4 expression. Finally, the TUG1 shRNA reduced the infarction area and cell apoptosis in I/R mouse brains in vivo. In summary, our results suggested that lncRNA TUG1 may function as a competing endogenous RNA (ceRNA) for miR‐145 to induce cell damage, possibly providing a new therapeutic target in cerebral ischaemia/reperfusion injury.

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MicroRNA-29b alleviates oxygen and glucose deprivation/reperfusion-induced injury via inhibition of the p53‑dependent apoptosis pathway in N2a neuroblastoma cells

Cited by 19 publications

References 45 publications

Retracted: MicroRNA‐132 protects H9c2 cells against oxygen and glucose deprivation‐evoked injury by targeting FOXO3A

Retracted: MicroRNA‐132 protects H9c2 cells against oxygen and glucose deprivation‐evoked injury by targeting FOXO3A

Deregulated miR-29b-3p Correlates with Tissue-Specific Activation of Intrinsic Apoptosis in An Animal Model of Amyotrophic Lateral Sclerosis

Long noncoding RNA TUG1 contributes to cerebral ischaemia/reperfusion injury by sponging mir‐145 to up‐regulate AQP4 expression

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