microRNA-183 Mediates Protective Postconditioning of the Liver by Repressing Apaf-1

Lin, Hui-Chen; Liu, Shin-Yun; Yen, Er-Yen; Li, Tsai-Kun; Lai, I-Rue

doi:10.1089/ars.2016.6679

Cited by 13 publications

(14 citation statements)

References 36 publications

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“…The predicted and verified target of miR-183 was SIRT1 and this target was bind with the 3 0 -UTR of miR-183-3p instead of miR-183-5p. miR-183-3p was widely reported in plenty of diseases, such as female lung cancer [23], endometriosis [24], and ischemia reperfusion injury [25]. Therefore, miR-183-3p was fully uncovered in this study.…”

Section: Discussionmentioning

confidence: 76%

RETRACTED ARTICLE: MicroRNA-183 affects the development of gastric cancer by regulating autophagy via MALAT1-miR-183-SIRT1 axis and PI3K/AKT/mTOR signals

Wang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Gastric cancer (GC) remains to be a familiar malignant tumor with poor prognosis and daunting impacts on global health. We planned to grab the latent impacts of microRNA-183 in regulating cell autophagy, thus to clarify its possible regulatory principle in GC. The miR-183 level in GC tissues and cell lines was investigated. The impacts of miR-183 dysregulation on cell biological performances including viability, apoptosis and autophagy of GC cell lines including SGC-7901 were detected. Also, cells were disposed with 3-methyladenine (3-MA, an autophagy inhibition) before dysregulation of miR-183 to further investigate the correlation between cell autophagy and viability or apoptosis. Furthermore, the regulatory mechanisms between miR-183 and metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), silent mating type information regulation 1 (SIRT1) or PI3K/AKT/mTOR pathway were explored. miR-183 was under-expressed both in GC tissues and in cell lines. miR-183 mimic alone depressed SGC-7901 cell viability and enhanced cell apoptosis and autophagy, whereas miR-183 inhibitor exhibited opposite effects. Moreover, the impacts of miR-183 on SGC-7901 cell viability and apoptosis were mediated by affecting the activation of autophagy. Our results indicate that miR-183 is under-expressed in GC cells and depression of miR-183 may enhance GC cell viability and inhibit cell apoptosis by affecting the activation of cell autophagy. MALAT1-miR-183-SIRT1 axis and PI3K/AKT/mTOR pathway may be mechanisms to mediate autophagy in GC. miR-183 may serve as a towardly therapeutic target for GC. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 76%

RETRACTED ARTICLE: MicroRNA-183 affects the development of gastric cancer by regulating autophagy via MALAT1-miR-183-SIRT1 axis and PI3K/AKT/mTOR signals

Wang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“… 19 miR-183 also have protective effect on ischemic liver injury. 20 These results suggest that modulation of miR-183 cluster could be a potential therapeutic approaches for the treatment of deafness.…”

Section: Discussionmentioning

confidence: 93%

microRNA-183 is Essential for Hair Cell Regeneration after Neomycin Injury in Zebrafish

Kim

Han

et al. 2018

Yonsei Med J

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PurposemicroRNAs (miRNAs) are non-coding RNAs composed of 20 to 22 nucleotides that regulate development and differentiation in various organs by silencing specific RNAs and regulating gene expression. In the present study, we show that the microRNA (miR)-183 cluster is upregulated during hair cell regeneration and that its inhibition reduces hair cell regeneration following neomycin-induced ototoxicity in zebrafish.Materials and MethodsmiRNA expression patterns after neomycin exposure were analyzed using microarray chips. Quantitative polymerase chain reaction was performed to validate miR-183 cluster expression patterns following neomycin exposure (500 µM for 2 h). After injection of an antisense morpholino (MO) to miR-183 (MO-183) immediately after fertilization, hair cell regeneration after neomycin exposure in neuromast cells was evaluated by fluorescent staining (YO-PRO1). The MO-183 effect also was assessed in transgenic zebrafish larvae expressing green fluorescent protein (GFP) in inner ear hair cells.ResultsMicroarray analysis clearly showed that the miR-183 cluster (miR-96, miR-182, and miR-183) was upregulated after neomycin treatment. We also confirmed upregulated expression of the miR-183 cluster during hair cell regeneration after neomycin-induced ototoxicity. miR-183 inhibition using MO-183 reduced hair cell regeneration in both wild-type and GFP transgenic zebrafish larvae.ConclusionOur work demonstrates that the miR-183 cluster is essential for the regeneration of hair cells following ototoxic injury in zebrafish larvae. Therefore, regulation of the miR-183 cluster can be a novel target for stimulation of hair cell regeneration.

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“…Zhang et al ( 29 ) have revealed that following transfection with miR-378 agomir, upregulation of miR-378 attenuated ischemic injury by negatively regulating the apoptosis-associated protein caspase-3. Although the regulation of miR-183 expression is considered to be effective for treating acute myocardial infarction or liver damage caused by ischemia ( 12 , 13 ), reports detailing miR-183 treatment in cerebral ischemia are unknown. As a member of the miR-183 gene cluster, the normal expression of miR-183-5p is important for nervous system function ( 30 ).…”

Section: Discussionmentioning

confidence: 99%

“…miR-183, which belongs to the evolutionarily conserved miRNA cluster, is located on human chromosome 7 and serves a number of functions in key cellular processes, including the development of neurons ( 11 ). Lin et al ( 12 ) have demonstrated that ischemic post-conditioning increases miR-183-5p levels in the murine liver compared with those in ischemia-reperfusion (I/R) mice. Furthermore, miR-183-5p upregulation alleviates liver injury after I/R by targeting apoptotic protease-activating factor 1.…”

Section: Introductionmentioning

confidence: 99%

miR‑183‑5p attenuates cerebral ischemia injury by negatively regulating PTEN

Zhu

Zhou

et al. 2020

Mol Med Rep

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cerebral ischemia is a common cerebrovascular disease caused by the occlusion of a cerebral blood vessel. Micrornas (mirnas/mirs) are emerging regulators of various human diseases, including cerebral ischemia. upregulation of mir-183-5p has been reported to alleviate liver injury induced by ischemia-reperfusion (i/r). However, the effect of mir-183-5p on cerebral ischemia injury remains unknown. The present study evaluated the effects of mir-183-5p on ischemia injury using ischemic models of mouse brains exposed to transient middle cerebral artery occlusion and neuro-2a (n2a) neuroblastoma cells exposed to oxygen-glucose-deprivation (oGd) and subsequently reoxygenated. ischemia was evaluated in mice using neurological function scores, cerebral edema, 2,3,5-triphenyltetrazoliumchloride, nissl and Fluoro-Jade B staining assays. in addition, mir-183-5p expression, n2a cell viability and the expression levels of apoptosis-associated proteins were detected by quantitative Pcr, cell counting Kit-8 assay, flow cytometry and western blotting. The association between mir-183-5p and phosphatase and tensin homolog (PTEN) was also confirmed by a luciferase reporter assay. The results revealed that mir-183-5p expression was decreased and brain damage was increased in ischemic mice compared with the sham group. additionally, mir-183-5p levels were reduced, and apoptosis was increased in n2a cells exposed to ischemia compared with the control group. Following transfection with agomir-183-5p, cerebral ischemic injury and apoptosis levels were reduced in the in vivo i/r stroke model and oGd-induced n2a cells. in addition, PTen was determined to be a target of mir-183-5p following elucidation of a direct binding site. overexpression of PTen reversed the mir-183-5p-induced n2a cell apoptosis inhibition and survival after oGd. The results of the present study suggested that mir-183-5p reduced ischemic injury by negatively regulating PTen, which may aid the development of a novel therapeutic strategy for cerebral ischemia.

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microRNA-183 Mediates Protective Postconditioning of the Liver by Repressing Apaf-1

Abstract: miR-183 mediated the tolerance induced by iPoC in livers via Apaf-1 repressing. Antioxid. Redox Signal. 26, 583-597.

Cited by 13 publications

References 36 publications

RETRACTED ARTICLE: MicroRNA-183 affects the development of gastric cancer by regulating autophagy via MALAT1-miR-183-SIRT1 axis and PI3K/AKT/mTOR signals

RETRACTED ARTICLE: MicroRNA-183 affects the development of gastric cancer by regulating autophagy via MALAT1-miR-183-SIRT1 axis and PI3K/AKT/mTOR signals

microRNA-183 is Essential for Hair Cell Regeneration after Neomycin Injury in Zebrafish

miR‑183‑5p attenuates cerebral ischemia injury by negatively regulating PTEN

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