Evidence map›Paper›PMID 33771972›Full record

ArticleTranslational psychiatry2021

PTEN in prefrontal cortex is essential in regulating depression-like behaviors in mice.

Xiao-Qing Wang, Lei Zhang, Zhong-Yuan Xia, Jia-Yin Chen, Yiru Fang, Yu-Qiang Ding

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 3 pooled it
3.1field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 3 syntheses or guidelines pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. AAV9-MediatedPharmaceutics · 2026
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  8. Establishment of a Depression Model Using Dexamethasone-treated Three-dimensional Cultured Rat Cortical Cells.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025
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  9. Article
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  12. Pentoxifylline Prevents Neuroinflammation and Modifies PTEN/TrkB Signaling in an LPS-Induced Depression Model.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Neural plasticity and depression treatment.IBRO neuroscience reports · 2023
    Article
  18. Review
  19. Suppressive Effects ofBiomedicines · 2023
    Article
  20. 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

6 authors at 3 institutions in 2 countries.

Xiao-Qing WangKey Laboratory of Arrhythmias, Ministry of Education of China, East Hospital, and Department of Anatomy and Neurobiology, Tongji University School of Medicine, Shanghai, 200092, China.
Lei ZhangKey Laboratory of Arrhythmias, Ministry of Education of China, East Hospital, and Department of Anatomy and Neurobiology, Tongji University School of Medicine, Shanghai, 200092, China. leizhang1120@outlook.com.ORCID 0000-0001-7242-5292
Zhong-Yuan XiaShanghai Tenth People's Hospital, Clinical Medical School of Nanjing Medical University, Nanjing, 211166, China.
Jia-Yin ChenKey Laboratory of Arrhythmias, Ministry of Education of China, East Hospital, and Department of Anatomy and Neurobiology, Tongji University School of Medicine, Shanghai, 200092, China.
Yiru FangClinical Research Center and Division of Mood Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.ORCID 0000-0002-8748-9085
Yu-Qiang DingKey Laboratory of Arrhythmias, Ministry of Education of China, East Hospital, and Department of Anatomy and Neurobiology, Tongji University School of Medicine, Shanghai, 200092, China. dingyuqiang@vip.163.com.ORCID 0000-0003-1202-4635
Tongji University · CNShanghai Jiao Tong University · CNShanghai Tenth People's Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31671061National Natural Science Foundation of China (National Science Foundation of China) 81930033National Natural Science Foundation of China (National Science Foundation of China) 91232724Science and Technology Commission of Shanghai Municipality (Shanghai Municipal Science and Technology Commission) 19490714300Science and Technology Commission of Shanghai Municipality (Shanghai Municipal Science and Technology Commission) 2018SHZDZX01Science and Technology Commission of Shanghai Municipality (Shanghai Municipal Science and Technology Commission) 2018SHZDZX05Science and Technology Commission of Shanghai Municipality (Shanghai Municipal Science and Technology Commission) 2020CXJQ01
6 · The paper itself

Abstract

Chronic stress is an environmental risk factor for depression and causes neuronal atrophy in the prefrontal cortex (PFC) and other brain regions. It is still unclear about the molecular mechanism underlying the behavioral alterations and neuronal atrophy induced by chronic stress. We here report that phosphatase and tensin homolog deleted on chromosome ten (PTEN) is a mediator for chronic stress-induced depression-like behaviors and neuronal atrophy in mice. One-month chronic restraint stress (CRS) up-regulated PTEN signaling pathway in the PFC of mice as indicated by increasing levels of PTEN, p-MEK, and p-ERK but decreasing levels of p-AKT. Over-expression of Pten in the PFC led to an increase of depression-like behaviors, whereas genetic inactivation or knockdown of Pten in the PFC prevented the CRS-induced depression-like behaviors. In addition, systemic administration of PTEN inhibitor was also able to prevent these behaviors. Cellular examination showed that Pten over-expression or the CRS treatment resulted in PFC neuron atrophy, and this atrophy was blocked by genetic inactivation of Pten or systemic administration of PTEN inhibitor. Furthermore, possible causal link between Pten and glucocorticoids was examined. In chronic dexamethasone (Dex, a glucocorticoid agonist) treatment-induced depression model, increased PTEN levels were observed, and depression-like behaviors and PFC neuron atrophy were attenuated by the administration of PTEN inhibitor. Our results indicate that PTEN serves as a key mediator in chronic stress-induced neuron atrophy as well as depression-like behaviors, providing molecular evidence supporting the synaptic plasticity theory of depression.

Indexed as

DepressionStress, PsychologicalAnimalsGlucocorticoidsMiceNeuronal PlasticityPrefrontal CortexGlucocorticoids

Identifiers

PMID33771972
PMCPMC7998021
OpenAlexW3139310007

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.