Evidence map›Paper›PMID 31760579›Full record

ArticleJournal of molecular neuroscience : MN2020

EDNRB Reverses Methylprednisolone-Mediated Decrease in Neural Progenitor Cell Viability via Regulating PI3K/Akt Pathway and lncRNA Expression.

Shiyuan Li, Ming Zeng, Lin Yang, Jianqi Yang, Jianshao Tan, Hongye Guan, Manyuan Kuang

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In one paragraph

Article in Journal of molecular neuroscience : MN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.1field-weighted citation impact, top 57% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

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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 1 institution in 1 country.

Shiyuan LiDepartment of Spinal Surgery, the First People's Hospital of Foshan, North Lingnan Avenue 81, Foshan, 528000, Guangdong, China. 214265029@qq.com.ORCID http://orcid.org/0000-0002-1073-349X
Ming ZengDepartment of Spinal Surgery, the First People's Hospital of Foshan, North Lingnan Avenue 81, Foshan, 528000, Guangdong, China.
Lin YangDepartment of Spinal Surgery, the First People's Hospital of Foshan, North Lingnan Avenue 81, Foshan, 528000, Guangdong, China.
Jianqi YangDepartment of Spinal Surgery, the First People's Hospital of Foshan, North Lingnan Avenue 81, Foshan, 528000, Guangdong, China.
Jianshao TanDepartment of Spinal Surgery, the First People's Hospital of Foshan, North Lingnan Avenue 81, Foshan, 528000, Guangdong, China.
Hongye GuanDepartment of Spinal Surgery, the First People's Hospital of Foshan, North Lingnan Avenue 81, Foshan, 528000, Guangdong, China.
Manyuan KuangDepartment of Spinal Surgery, the First People's Hospital of Foshan, North Lingnan Avenue 81, Foshan, 528000, Guangdong, China.
First People's Hospital of Foshan · CN

Funding

Natural Science Foundation of Guangdong Province 2015A030310376
6 · The paper itself

Abstract

objectiveTo investigate the functions and mechanisms of methylprednisolone (MP) through endothelin receptor B (EDNRB) on the cell proliferation of neural progenitor cells (NPCs) to regulate spinal cord injury.

methodsPrimary NPCs were isolated from fetal mice and subjected to treatments with MP and IRL-1620 (EDNRB agonist). The cell viability was determined using the MTS assay. Total RNA was extracted from the cells, and RNA-seq was performed to screen for lncRNAs. The targets of the candidate lncRNAs were predicted by GO and KEGG analyses, and the expressions of lncRNAs were validated via qPCR. Furthermore, protein levels of the PI3K-AKT pathway were determined via Western blotting, and the expression of lncRNAs was detected after inhibiting the pathway with AKT inhibitor.

resultsMTS assays revealed that MP decreased the cell viability of NPCs, whereas the EDNRB agonist reversed this effect of MP. NPCs were used for RNA-seq in the following three groups: normal control (NC), MP, and MP combined with EDNRB agonist (MP + EDNRB). Our results suggested that the NONRATT030699.2, NONRATT004088.2, and NONRATT005601.2 lncRNAs might be involved in the signaling pathway that is correlated to MP and the EDNRB agonist. GO and KEGG pathway analyses revealed that this was the PI3K/AKT pathway. The relevant genes involved in the pathway were validated by Western blotting. The EDNRB agonist promoted cell proliferation mainly via the activation of the PI3K/AKT pathway; however, it suppressed the expression of p-ERK, thereby increasing the expression of cyclin D1 and attenuating the effect of MP in suppressing cell proliferation. Meanwhile, after the AKT signal pathway was inhibited, these lncRNA expressions were consistent with those in the MP + EDNRB group.

conclusionMP inhibits NPC proliferation, whereas EDNRB activation reverses the effect of MP via lncRNA.

Indexed as

Signal TransductionAnimalsCell ProliferationCells, CulturedCell SurvivalMethylprednisoloneNeural Stem CellsNeuroprotective AgentsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyReceptor, Endothelin BRNA, Long Noncodingednrb protein, ratMethylprednisoloneNeuroprotective AgentsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, Endothelin BRNA, Long NoncodingEDNRBMethylprednisoloneNeural progenitor cellsSpinal cord injury

Identifiers

PMID31760579
OpenAlexW2990668175

What OpenQuestion holds

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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.