miRNA-223 regulates ischemic neuronal injury by targeting the type 1 insulin-like growth factor receptor (IGF1R)

Feng, She-Jun; Zhang, Xueqiang; Li, Juntao; Dai, Xiao-Qing; Zhao, Fei

doi:10.5114/fn.2018.74659

Cited by 21 publications

(16 citation statements)

References 25 publications

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“…The biological function of FGD5-AS1 in stroke remains unclear. In our present study, FGD5-AS1 is predicted and demonstrated as a ceRNA for miR-223, which has been reported to involve in OGD/R-induced neurons injury by regulat- ing IGF1R [5]. The expression of miR-223 was negatively regulated by FGD5-AS1 as we found that overexpression of FGD5-AS1 significantly decreases the level of miR-223.…”

Section: Discussionsupporting

confidence: 67%

“…In our previous study, the involvement of miR-223/IGF1R in OGD/R-induced neuron injury has been proved. MiR-223 was illustrated to exhibit an inhibitory effect on the prolif-eration of OGD/R-injured neurons via retarding IGF1R expression [5]. Here, lncRNA FGD5-AS1 was forecasted and verified as a ceRNA for miR-223.…”

Section: Discussionmentioning

confidence: 93%

“…The OGD/R model was established as per our previous description [5]. In brief, the primary cortical neurons were cultured in glucose-free Earle's balanced salt solution (BSS) in an anaerobic incubator with 95% N 2 and 5% CO 2 at 37°C.…”

Section: Materials and Methods Primary Cortical Neuron Isolation And Omentioning

confidence: 99%

“…Western blot was performed as described previously [5]. The protein bands were detected using an enhanced chemiluminescence detection kit (ECL, Pierce Biotechnology Inc.).…”

Section: Western Blotmentioning

confidence: 99%

“…In a previous study, it was identified that miR-223 was over-expressed in neurons suffering from oxygen-glucose deprivation and simulated reperfusion (OGD/R) and it suppressed the growth of OGD/Rinjured neurons by repressing insulin-like growth factor-1 receptor (IGF1R) expression [5]. IGF1R is known as a transmembrane receptor tyrosine kinase which is implicated in the regulation of IGF bioactivity [13].…”

Section: Introductionmentioning

confidence: 99%

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LncRNA FGD5-AS1 acts as a competing endogenous RNA for miRNA-223 to lessen oxygen-glucose deprivation and simulated reperfusion (OGD/R)-induced neurons injury

Zhang¹,

Song²,

Feng³

et al. 2019

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The purpose of this study was to evaluate whether FGD5-AS1 participates in oxygen-glucose deprivation and simulated reperfusion (OGD/R)-induced neurons injury and the detailed mechanism. An OGD/R model was established using the primary cortical neuron isolated from the brains of Sprague-Dawley rats. qRT-PCR and western blot were performed to detect the RNA and protein expression levels, respectively. Cell counting kit 8 (CCK8) and flow cytometry assays were used to evaluate the proliferation and apoptosis of neurons. The luciferase reporter assay was used to verify the interaction between lncRNA FGD5-AS1 and miRNA-223. We found that the expression of FGD5-AS1 is decreased in neurons suffering from OGD/R. Up-regulation of FGD5-AS1 could recover proliferation and inhibit apoptosis of OGD/R-injured neurons. In addition, the interaction between FGD5-AS1 and miRNA-223 were verified. The expression of miRNA-223 was negatively correlated with the level of FGD5-AS1. In turn, the expression of insulin-like growth factor-1 receptor (IGFIR, a target gene of miR-223) was positively associated with the level of FGD5-AS1. Simultaneously down-regulating miR-223 and over-expressing FGD5-AS1 as well as IGF1R exhibited an additional effect of extenuating OGD/R damage i.e. increasing neuron proliferation and reducing neuron apoptosis. In conclusion, our findings indicated that FGD5-AS1 may protect the neuron against OGD/R injury via acting as a ceRNA for miR-223 to mediate IGF1R expression, which contributes to a deeper understanding of ischemic stroke and provide a promising therapeutic target for this disease.

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Section: Discussionsupporting

confidence: 67%

Section: Discussionmentioning

confidence: 93%

Section: Materials and Methods Primary Cortical Neuron Isolation And Omentioning

confidence: 99%

“…Western blot was performed as described previously [5]. The protein bands were detected using an enhanced chemiluminescence detection kit (ECL, Pierce Biotechnology Inc.).…”

Section: Western Blotmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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LncRNA FGD5-AS1 acts as a competing endogenous RNA for miRNA-223 to lessen oxygen-glucose deprivation and simulated reperfusion (OGD/R)-induced neurons injury

Zhang¹,

Song²,

Feng³

et al. 2019

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In vivo targeting of miR‐223 in experimental eosinophilic oesophagitis

et al. 2020

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Objectives Eosinophilic oesophagitis (EoE) is characterised by oesophageal inflammation, fibrosis and dysfunction. Micro (mi)‐RNAs interfere with pro‐inflammatory and pro‐fibrotic transcriptional programs, and miR‐223 was upregulated in oesophageal mucosal biopsy specimens from EoE patients. The therapeutic potential of modulating miR‐223 expression in vivo has not been determined. We aimed to elucidate the relevance of oesophageal miR‐223 expression in an in vivo model of EoE by inhibiting miR‐223 tissue expression. Methods The expression of miR‐223 and the validated miR‐223 target insulin‐like growth factor receptor 1 (IGF1R) protein was determined in our paediatric cohort of EoE patients. A murine model of Aspergillus fumigatus‐induced EoE was employed, and oesophagi were assessed for miR‐233, IGF1R, T lymphocyte type 2 (T2) cytokine expression and eosinophil infiltration. Mice were treated with antagomirs targeting miR‐223 or resveratrol targeting its upstream regulator Midline‐1(MID‐1). Results There was an inverse relationship between an increased expression of miR‐223 and a decreased IGF1R protein concentration in biopsy specimens from EoE patients. TNF‐related apoptosis‐inducing ligand deficiency, MID‐1 inhibition and resveratrol treatment suppressed miR‐223 expression. Furthermore, inhibition of miR‐223 and treatment with resveratrol in the oesophagus resulted in an amelioration of EoE hallmark features including eosinophilic infiltration, oesophageal circumference and a reduction in T2 cytokine expression. Conclusion miR‐223 has a key role in the perpetuation of EoE hallmark features downstream of TNF‐related apoptosis‐inducing ligand and MID‐1 in an experimental model. These studies highlight a potentially critical role of miRNA function in EoE aetiology. miR‐223 expression in the oesophagus may be therapeutically modulated by resveratrol, providing a potential new therapeutic option to be explored in EoE patients for this increasingly prevalent condition.

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Possible Involvement of Hippocampal miR‐539‐3p/Lrp6/Igf1r Axis for Diminished Working Memory in Mice Fed a Low‐Carbohydrate and High‐Protein Diet

Shima,

Onishi,

Terashima

2024

Molecular Nutrition Food Res

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A low‐carbohydrate and high‐protein (LC‐HP) diet demonstrates favorable impacts on metabolic parameters, albeit it leads to a decline in hippocampal function with the decreased expression of hippocampal insulin‐like growth factor‐1 receptor (IGF‐1R) among healthy mice. However, the precise mechanisms underlying this phenomenon remain unexplored. Eight‐week‐old male C57BL/6 mice were divided into the LC‐HP diet‐fed group (25.1% carbohydrate, 57.2% protein, and 17.7% fat as percentages of calories; n = 10) and the control diet‐fed group (58.9% carbohydrate, 24.0% protein, and 17.1% fat; n = 10). After 4 weeks, all mice underwent the Y‐maze test, followed by analyses of hippocampal mRNA and miRNA expressions. We revealed that feeding the LC‐HP diet suppressed working memory function and hippocampal Igf1r mRNA levels in mice. Sequencing of hippocampal miRNA demonstrated 17 upregulated and 27 downregulated miRNAs in the LC‐HP diet‐fed mice. Notably, we found decreased hippocampal mRNA levels of low‐density lipoprotein receptor‐related protein 6 (Lrp6), a gene modulated by miR‐539‐3p, in mice fed the LC‐HP diet. Furthermore, a significant positive correlation was observed between Lrp6 and Igf1r mRNA levels in the hippocampus. These findings suggest that LC‐HP diets may suppress hippocampal function via the miR‐539‐3p/Lrp6/Igf1r axis.

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miRNA-223 regulates ischemic neuronal injury by targeting the type 1 insulin-like growth factor receptor (IGF1R)

Cited by 21 publications

References 25 publications

LncRNA FGD5-AS1 acts as a competing endogenous RNA for miRNA-223 to lessen oxygen-glucose deprivation and simulated reperfusion (OGD/R)-induced neurons injury

LncRNA FGD5-AS1 acts as a competing endogenous RNA for miRNA-223 to lessen oxygen-glucose deprivation and simulated reperfusion (OGD/R)-induced neurons injury

In vivo targeting of miR‐223 in experimental eosinophilic oesophagitis

Possible Involvement of Hippocampal miR‐539‐3p/Lrp6/Igf1r Axis for Diminished Working Memory in Mice Fed a Low‐Carbohydrate and High‐Protein Diet

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