Micro<scp>RNA</scp>‐211 causes ganglion cell dysplasia in congenital intestinal atresia via down‐regulation of glial‐derived neurotrophic factor

Xia, Ziqiang; Ding, Daokui; Zhang, N.; Wang, J.-x.; Yang, Heying; Zhang, Depei

doi:10.1111/nmo.12705

Cited by 12 publications

(9 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…miRNA-211 is also reported to regulate glial-derived neurotrophic factor, a neurotrophic factor and key neurotrophin in the enteric nervous system (ENS). 34 In our study, we found that miR-211-5p was downregulated in the hippocampus of SHRs. Many studies have shown that Dyrk1a is a protein-coding gene that is closely related to the development and function of the brain.…”

Section: Discussionsupporting

confidence: 53%

miRNA profiling in the hippocampus of attention‐deficit/hyperactivity disorder rats

Tian

Zhang

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

Attention-deficit/hyperactivity disorder (ADHD) is characterized by attention deficit, hyperactivity, impulsivity, and learning and memory impairment.Although the pathogenesis of learning and memory impairment is still unknown, some studies have suggested an association with hippocampus dysfunction. We aimed to explore the role of miRNAs in the learning and memory impairments observed in ADHD. Differentially expressed hippocampal micro-ribonucleic acids (miRNAs) in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto rats (WKYs) were detected on an Illumina HiSeq. 2000 genome analyzer. A total of 25 differentially expressed miRNAs (fold-change ≥ 2 and P-value < 0.05) were identified. The target genes of these differentially expressed miRNAs were predicted using online tools (TargetScan and miRDB). Gene ontology and pathway analysis of the predicted target genes were carried out to assess their putative biological functions. Meanwhile, quantitative realtime PCR was used to validate the HiSeq results, revealing that three miRNAs (miR-1-b, miR-741-3p, and miR-206-3p) were upregulated and four (miR-182, miR-471-5p, miR-183-5p, and miR-211-5p) were downregulated in the SHR group compared with the WKY group. In addition, we confirmed that Dyrk1a is regulated by miR-211-5p. These results help us understand the contribution of miRNAs in the hippocampus to ADHD and provide new insights into the pathogenesis of this condition. K E Y W O R D S attention-deficit/hyperactivity disorder (ADHD), high-throughput sequencing, microRNA (miRNAs), spontaneously hypertensive rat (SHR), Wistar-Kyoto rat (WKY) J Cell Biochem. 2019;120:3621-3629.wileyonlinelibrary.com/journal/jcb

show abstract

Section: Discussionsupporting

confidence: 53%

miRNA profiling in the hippocampus of attention‐deficit/hyperactivity disorder rats

Tian

Zhang

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

show abstract

“…miR-211 is a neuron-related miRNA that can inhibit neuronal differentiation in Alzheimer's disease [24]. Xia et al found that GDNF was a target of miR-211, and GDNF was negatively regulated by miR-211 in retinal ganglion cells [25]. Moreover, bioinformatics software predicted the binding sites between MIAT and miR-211.…”

Section: Introductionmentioning

confidence: 99%

LncRNA MIAT overexpression reduced neuron apoptosis in a neonatal rat model of hypoxic-ischemic injury through miR-211/GDNF

Zhao

Jian

et al. 2018

Cell Cycle

View full text Add to dashboard Cite

Objective: To investigate the underlying mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in hypoxic-ischemic (HI)-induced neonatal cerebral palsy. Materials and methods: Neonatal rat model of HI injury was established to detect the motor function. LncRNA MIAT, miR-211, glial cell line-derived neurotrophic factor (GDNF) and caspase-3 expressions were measured by qRT-PCR or western blot. The apoptosis of Neuro2A cells was detected by flow cytometry. RNA immunoprecipitation (RIP) and RNA pull-down assays were performed to confirm the interaction between MIAT and miR-211. Results: Compared with control group, lncRNA MIAT and GDNF were downregulated in striatal tissues of neonatal rats in HI group and oxygen glucose deprivation (OGD)-induced ischemic injury of Neuro2A cells, whereas miR-211 was up-regulated in striatal tissues of HI group and OGDinduced ischemic injury of Neuro2A cells. LncRNA MIAT interacted with miR-211, and lncRNA MIAT overexpression reduced neuron apoptosis through miR-211. Besides, GDNF expression was positively regulated by lncRNA MIAT and negatively regulated by miR-211 in Neuro2A cells. In vivo experiment proved MIAT promoted motor function and relieved HI injury. Conclusion: MIAT overexpression reduced apoptosis of Neuro2A cells through miR-211/GDNF, which relieved HI injury of neonatal rats.

show abstract

“…GDNF homeostasis is likely more complex and involves regulation at several non-transcriptomic levels ( d’Anglemont de Tassigny et al , 2015 ). For instance, Gdnf mRNA degradation is highly regulated by microRNAs ( Kumar et al , 2015 ; Xia et al , 2016 ; Zhang et al , 2019 ). However, a low basal level of expression is probably necessary to prevent over-activation of dopaminergic terminals and deleterious effects of GDNF.…”

Section: Discussionmentioning

confidence: 99%

Molecular targets for endogenous glial cell line-derived neurotrophic factor modulation in striatal parvalbumin interneurons

Enterría‐Morales

provided

Blesa

et al. 2020

Brain Communications

View full text Add to dashboard Cite

Administration of recombinant glial cell line-derived neurotrophic factor (GDNF) into the putamen has been tested in preclinical and clinical studies to evaluate its neuroprotective effects on the progressive dopaminergic neuronal degeneration that characterises Parkinson’s disease. However, intracerebral GDNF infusion is a challenging therapeutic strategy, with numerous potential technical and medical limitations. Most of these limitations could be avoided if the production of endogenous GDNF could be increased. GDNF is naturally produced in the striatum from where it exerts a trophic action on the nigrostriatal dopaminergic pathway. Most of striatal GDNF is synthesized by a subset of GABAergic interneurons characterised by the expression of parvalbumin. We sought to identify molecular targets specific to those neurons and which are putatively associated with GDNF synthesis. To this end, the transcriptomic differences between GDNF-positive parvalbumin neurons in the striatum and parvalbumin neurons located in the nearby cortex, which do not express GDNF, were analysed. Using mouse reporter models, we have defined the genomic signature of striatal parvalbumin interneurons obtained by fluorescence-activated cell sorting followed by microarray comparison. Short-listed genes were validated by additional histological and molecular analyses. These genes code for membrane receptors (Kit, Gpr83, Tacr1, Tacr3, Mc3r), cytosolic proteins (Pde3a, Crabp1, Rarres2, Moxd1), and a transcription factor (Lhx8). We also found the proto-oncogene cKit to be highly specific of parvalbumin interneurons in the nonhuman primate striatum, thus highlighting a conserved expression between species and suggesting that specific genes identified in mouse parvalbumin neurons could be putative targets in the human brain. Pharmacological stimulation of four G-protein coupled receptors enriched in the striatal parvalbumin interneurons inhibited Gdnf expression presumably by decreasing cyclic adenosine monophosphate formation. Additional experiments with pharmacological modulators of adenylyl cyclase and protein kinase A indicated that this pathway is a relevant intracellular route to induce Gdnf gene activation. This preclinical study is an important step in the ongoing development of a specific pro-endo-GDNF pharmacological strategy to treat Parkinson’s disease.

show abstract

MicroRNA‐211 causes ganglion cell dysplasia in congenital intestinal atresia via down‐regulation of glial‐derived neurotrophic factor

Abstract: Our results indicate that overexpression of miR-211 suppresses the differentiation of BMSCs into intestinal ganglion cells by directly down-regulating the expression of GDNF. The findings elucidate the role of miRNA in congenital intestinal atresia.

Cited by 12 publications

References 28 publications

miRNA profiling in the hippocampus of attention‐deficit/hyperactivity disorder rats

miRNA profiling in the hippocampus of attention‐deficit/hyperactivity disorder rats

LncRNA MIAT overexpression reduced neuron apoptosis in a neonatal rat model of hypoxic-ischemic injury through miR-211/GDNF

Molecular targets for endogenous glial cell line-derived neurotrophic factor modulation in striatal parvalbumin interneurons

Contact Info

Product

Resources

About