Evidence map›Paper›PMID 27647309›Full record

ArticleJournal of molecular neuroscience : MN2016

Thrombospondin-4 Promotes Neuronal Differentiation of NG2 Cells via the ERK/MAPK Pathway.

Hai Jie Yang, Shuang Ping Ma, Fei Ju, Ya Ping Zhang, Zhi Chao Li, Bin Bin Zhang, Jun Jiang Lian, Lei Wang, Bin Feng Cheng, Mian Wang and 1 more

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
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  6. Article
  7. Thrombospondin-4 in tissue remodeling.Matrix biology : journal of the International Society for Matrix Biology · 2019
    Review
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  9. Review
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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

11 authors at 2 institutions in 1 country.

Hai Jie YangSchool of Life Science and Technology, Xinxiang Medical University, Xinxiang, China. hjyang_wmd@hotmail.com.
Shuang Ping MaSchool of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Fei JuSchool of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Ya Ping ZhangSchool of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Zhi Chao LiSchool of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Bin Bin ZhangSchool of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Jun Jiang LianSchool of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Lei WangSchool of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Bin Feng ChengSchool of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Mian WangSchool of Life Science and Technology, Xinxiang Medical University, Xinxiang, China. xxyxy_wm@163.com.
Zhi Wei FengSchool of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Xinxiang Medical University · CNHenan Psychiatric Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NG2-expressing neural progenitors can produce neurons in the central nervous system, providing a potential cell resource of therapy for neurological disorders. However, the mechanism underlying neuronal differentiation of NG2 cells remains largely unknown. In this report, we found that a thrombospondin (TSP) family member, TSP4, is involved in the neuronal differentiation of NG2 cells. When TSP4 was overexpressed, NG2 cells underwent spontaneous neuronal differentiation, as demonstrated by the induction of various neuronal differentiation markers such as NeuN, Tuj1, and NF200, at the messenger RNA and protein levels. In contrast, TSP4 silencing had an opposite effect on the expression of neuronal differentiation markers in NG2 cells. Next, the signaling pathway responsible for TSP4-mediated NG2 cell differentiation was investigated. We found that ERK but not p38 and AKT signaling was affected by TSP4 overexpression. Furthermore, when ERK signaling was blocked by the inhibitor U0126, the neuronal marker expression of NG2 cells was substantially increased. Together, these findings suggested that TSP4 promoted neuronal differentiation of NG2 cells by inhibiting ERK/MAPK signaling, revealing a novel role of TSP4 in cell fate specification of NG2 cells.

Indexed as

MAP Kinase Signaling SystemNeurogenesisAnimalsAntigens, NuclearCell LineNerve Tissue ProteinsNeurofilament ProteinsNeuronsp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktRatsThrombospondinsTubulinAntigens, NuclearNerve Tissue ProteinsNeurofilament Proteinsp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktRbfox3 protein, ratthrombospondin 4ThrombospondinsTubulinCell therapyNeuronal differentiationNG2 cellsSignaling pathwayThrombospondin-4

Identifiers

PMID27647309
OpenAlexW2523441459

What OpenQuestion holds

Textmetadata
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.