Evidence map›Paper›PMID 29209172›Full record

ArticleFrontiers in cellular neuroscience2017

The Role of Netrin-1 in Improving Functional Recovery through Autophagy Stimulation Following Spinal Cord Injury in Rats.

Liangjie Bai, Xifan Mei, Yanfeng Wang, Yajiang Yuan, Yunlong Bi, Gang Li, Hongyu Wang, Peng Yan, Gang Lv

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 15% 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, 36 citations in OpenAlex.

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  17. Spinal AMP kinase activity differentially regulates phrenic motor plasticity.Journal of applied physiology (Bethesda, Md. : 1985) · 2020
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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

9 authors at 3 institutions in 1 country.

Liangjie BaiDepartment of Orthopedics, The First Affiliated Hospital of China Medical University, Shenyang, China.
Xifan MeiDepartment of Orthopedics, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China.
Yanfeng WangDepartment of Orthopedics, The First Affiliated Hospital of China Medical University, Shenyang, China.
Yajiang YuanDepartment of Orthopedics, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China.
Yunlong BiDepartment of Orthopedics, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China.
Gang LiDepartment of Orthopedics, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China.
Hongyu WangDepartment of Orthopedics, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China.
Peng YanDepartment of Orthopedics, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China.
Gang LvDepartment of Orthopedics, The First Affiliated Hospital of China Medical University, Shenyang, China.
Jinzhou Medical University · CNFirst Hospital of China Medical University · CNChina Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous findings indicated that treatment with Netrin-1 could improve functional recovery through the stimulation of autophagy, by activating the AMP-activated protein kinase/mammalian target of rapamycin (AMPK/mTOR) signaling pathway in rats following spinal cord injury (SCI). However, the underlying mechanisms were not elucidated. The purpose of this study was to investigate the underlying mechanisms by which Netrin-1 promotes autophagy and improves functional recovery after SCI. Following controlled SCI in Sprague-Dawley rats, we observed that the autophagic flux in neurons was impaired, as reflected by the accumulation of light chain 3-II (LC3-II)-positive and LC3-positive autophagosomes (APs), accompanied by the accumulation of the autophagic substrate, Sequestosome 1 (SQSTM1; also known as p62). Our results showed that treatment with Netrin-1 increases the levels of the lysosomal protease cathepsin D (CTSD) and lysosomal-associated membrane protein 1 (LAMP1), through the regulation of the nuclear localization of Transcription factor EB (TFEB) via the AMPK/mTOR signaling pathway. In addition, this enhancement of lysosomal biogenesis correlated strongly with the restoration of autophagic flux, inhibition of neural apoptosis and improved functional recovery. Suppression of lysosomal biogenesis via the inhibition of the nuclear translocation of TFEB by Compound C abolished this restoration of autophagic flux and the functional recovery effects of Netrin-1 following SCI. Taken together, these results indicate that Netrin-1 enhances lysosomal biogenesis by regulating the nuclear translocation of TFEB via the AMPK/mTOR signaling pathway. Furthermore, the enhancement of lysosomal biogenesis by Netrin-1 following SCI promotes autophagic flux and improves functional recovery in rats. Thus, the regulation of lysosomal biogenesis by modulating the nuclear localization of TFEB might be a novel approach for the treatment of SCI.

Indexed as

AMPKapoptosisautophagic fluxmTORNetrin-1spinal cord injurytranscription factor EB

Identifiers

PMID29209172
PMCPMC5701630
OpenAlexW2765897981

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LicenceCC BY
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Registered trials

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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.