Evidence map›Paper›PMID 27895121›Full record

ArticleThe Journal of biological chemistry2017

Neuronal mTORC1 Is Required for Maintaining the Nonreactive State of Astrocytes.

Yue Zhang, Song Xu, Kang-Yan Liang, Kai Li, Zhi-Peng Zou, Cui-Lan Yang, Kang Tan, Xiong Cao, Yu Jiang, Tian-Ming Gao and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

21 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  12. Brain-derived estrogen and neural function.Neuroscience and biobehavioral reviews · 2022
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Neuron-Derived Estrogen Is Critical for Astrocyte Activation and Neuroprotection of the Ischemic Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  18. Review
  19. Article
  20. Activation of autophagy rescues synaptic and cognitive deficits in fragile X mice.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
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 3 institutions in 2 countries.

Yue ZhangFrom the Academy of Orthopedics, Guangdong Province, the Third Affiliated Hospital, Southern Medical University, Guangzhou 510515, China.
Song XuFrom the Academy of Orthopedics, Guangdong Province, the Third Affiliated Hospital, Southern Medical University, Guangzhou 510515, China.
Kang-Yan Liangthe Department of Cell Biology, School of Basic Medical Science, Southern Medical University, Guangzhou 510515, China.
Kai Lithe Department of Cell Biology, School of Basic Medical Science, Southern Medical University, Guangzhou 510515, China.
Zhi-Peng Zouthe Department of Cell Biology, School of Basic Medical Science, Southern Medical University, Guangzhou 510515, China.
Cui-Lan Yangthe Department of Cell Biology, School of Basic Medical Science, Southern Medical University, Guangzhou 510515, China.
Kang Tanthe Department of Cell Biology, School of Basic Medical Science, Southern Medical University, Guangzhou 510515, China.
Xiong Caothe Department of Neurobiology, School of Basic Medical Science, Southern Medical University, Guangzhou 510515, China, and.
Yu Jiangthe Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213.
Tian-Ming Gaothe Department of Neurobiology, School of Basic Medical Science, Southern Medical University, Guangzhou 510515, China, and.
Xiao-Chun BaiFrom the Academy of Orthopedics, Guangdong Province, the Third Affiliated Hospital, Southern Medical University, Guangzhou 510515, China, baixc15@smu.edu.cn xiaochunbai@aliyun.com.
Southern Medical University · CNThird Affiliated Hospital of Southern Medical University · CNUniversity of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Astrocytes respond to CNS insults through reactive astrogliosis, but the underlying mechanisms are unclear. In this study, we show that inactivation of mechanistic target of rapamycin complex (mTORC1) signaling in postnatal neurons induces reactive astrogliosis in mice. Ablation of Raptor (an mTORC1-specific component) in postmitotic neurons abolished mTORC1 activity and produced neurons with smaller soma and fewer dendrites, resulting in microcephaly and aberrant behavior in adult mice. Interestingly, extensive astrogliosis without significant astrocyte proliferation and glial scar formation was observed in these mice. The inhibition of neuronal mTORC1 may activate astrogliosis by reducing neuron-derived fibroblast growth factor 2 (FGF-2), which might trigger FGF receptor signaling in astrocytes to maintain their nonreactive state, and FGF-2 injection successfully prevented astrogliosis in Raptor knock-out mice. This study demonstrates that neuronal mTORC1 inhibits reactive astrogliosis and plays an important role in CNS pathologies.

Indexed as

AnimalsAnimals, NewbornAstrocytesBehavior, AnimalCells, CulturedDendritesGliosisMechanistic Target of Rapamycin Complex 1MiceMice, KnockoutMultiprotein ComplexesNeurogliaNeuronsSignal TransductionTOR Serine-Threonine KinasesMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesTOR Serine-Threonine Kinasesastrocytefibroblast growth factor 2fibroblast growth factor (FGF)mammalian target of rapamycin (mTOR)mTOR complex (mTORC)neuronRaptorreactive astrogliosis

Identifiers

PMID27895121
PMCPMC5217670
OpenAlexW2559004720

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.