Evidence map›Paper›PMID 29637443›Full record

ArticleMolecular neurobiology2018

MiR-34a Regulates Axonal Growth of Dorsal Root Ganglia Neurons by Targeting FOXP2 and VAT1 in Postnatal and Adult Mouse.

Longfei Jia, Michael Chopp, Lei Wang, Xuerong Lu, Yi Zhang, Alexandra Szalad, Zheng Gang Zhang

Open access · greenAbstract read
In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

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  19. miR-34a in Neurophysiology and Neuropathology.Journal of molecular neuroscience : MN · 2019
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Longfei JiaDepartment of Neurology, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI, 48202, USA.
Michael ChoppDepartment of Neurology, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI, 48202, USA.
Lei WangDepartment of Neurology, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI, 48202, USA.
Xuerong LuDepartment of Neurology, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI, 48202, USA.
Yi ZhangDepartment of Neurology, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI, 48202, USA.
Alexandra SzaladDepartment of Neurology, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI, 48202, USA.
Zheng Gang ZhangDepartment of Neurology, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI, 48202, USA. zhazh@neuro.hfh.edu.ORCID http://orcid.org/0000-0002-3752-9894
Henry Ford Hospital · USCapital Medical University · CNOakland University · US

Funding

MicroRNAs and neurogenesis after strokeR01NS075156 · NINDS · HENRY FORD HEALTH SYSTEM · PI ZHANG, ZHENG GANG · 2011 to 2015
$1.6M
Thymosin Beta4 Promotes the Recovery of Peripheral neuropathy in Type II DiabeticR01DK097519 · NIDDK · HENRY FORD HEALTH SYSTEM · PI WANG, LEI · 2013 to 2016
$1.3M
PDE5 is a Therapeutic Target for Peripheral Neuropathy in Diabetic MiceR01NS075084 · NINDS · HENRY FORD HEALTH SYSTEM · PI WANG, LEI · 2012 to 2015
$1.3M
National Institute of Neurological Disorders and Stroke R01 NS075084National Institute of Neurological Disorders and Stroke RO1 NS075156NIDDK NIH HHS R01 DK097519NINDS NIH HHS R01 NS075084NINDS NIH HHS R01 NS075156
6 · The paper itself

Abstract

Hyperglycemia impairs nerve fibers of dorsal root ganglia (DRG) neurons, leading to diabetic peripheral neuropathy (DPN). However, the molecular mechanisms underlying DPN are not fully understood. Using a mouse model of type II diabetes (db/db mouse), we found that microRNA-34a (miR-34a) was over-expressed in DRG, sciatic nerve, and foot pad tissues of db/db mice. In vitro, high glucose significantly upregulated miR-34a in postnatal and adult DRG neurons, which was associated with inhibition of axonal growth. Overexpression and attenuation of miR-34a in postnatal and adult DRG neurons suppressed and promoted, respectively, axonal growth. Bioinformatic analysis suggested that miR-34a putatively targets forkhead box protein P2 (FOXP2) and vesicle amine transport 1 (VAT1), which were decreased in diabetic tissues and in cultured DRG neurons under high glucose conditions. Dual-luciferase assay showed that miR-34a downregulated FOXP2 and VAT1 expression by targeting their 3' UTR. Gain-of- and loss-of-function analysis showed an inverse relation between augmentation of miR-34a and reduction of FOXP2 and VAT1 proteins in postnatal and adult DRG neurons. Knockdown of FOXP2 and VAT1 reduced axonal growth. Together, these findings suggest that miR-34a and its target genes of FOXP2 and VAT1 are involved in DRG neuron damage under hyperglycemia.

Indexed as

3' Untranslated RegionsAnimalsAnimals, NewbornAxonsBase SequenceCell ProliferationCells, CulturedDiabetes Mellitus, ExperimentalForkhead Transcription FactorsGanglia, SpinalHyperglycemiaMice, Inbred C57BLMicroRNAsRepressor ProteinsVesicular Transport Proteins3' Untranslated RegionsForkhead Transcription FactorsFoxp2 protein, mouseMicroRNAsMIRN34a microRNA, mouseRepressor ProteinsVesicular Transport ProteinsAxon growthmiR-34aNeuronPeripheral neuropathy

Identifiers

PMID29637443
PMCPMC6179937
OpenAlexW2797358570

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.