Evidence map›Paper›PMID 32413560›Full record

ArticleBrain, behavior, and immunity2020

Analysis of cerebrovascular dysfunction caused by chronic social defeat in mice.

Michael L Lehmann, Chelsie N Poffenberger, Abdel G Elkahloun, Miles Herkenham

Open access · hybridAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 56 citations in OpenAlex.

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  14. Social stress induces autoimmune responses against the brain.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

4 authors at 2 institutions in 1 country.

Michael L LehmannSection on Functional Neuroanatomy, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: lehmannm@mail.nih.gov.
Chelsie N PoffenbergerSection on Functional Neuroanatomy, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA.
Abdel G ElkahlounDivision of Intramural Research Programs Microarray Core Facility, National Institutes of Health, Bethesda, MD 20892, USA.
Miles HerkenhamSection on Functional Neuroanatomy, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA.
National Institute of Mental Health · USNational Institutes of Health · US

Funding

Studies Of Central Nervous System Functional AnatomyZIAMH001090 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI HERKENHAM, MILES A. · 2009 to 2022
$19.3M
NHGRI/DIR Microarray CoreZICHG200365 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI ELKAHLOUN, ABDEL · 2011 to 2025
$9.0M
Intramural NIH HHS ZIA MH001090
6 · The paper itself

Abstract

Psychological stress and affective disorders are clinically associated with hypertension and vascular disease, but the biological links between the conditions have not been fully explored. To examine this relationship, we used chronic social defeat (CSD) stress, which produces anxiety-like and depressive-like behavioral declines in susceptible mice. In such mice, CSD also produces cerebrovascular microbleeds in scattered locations. Here, we showed further evidence of vascular pathology and blood-brain barrier breakdown by visualizing plasma immunoglobulins and erythrocytes within the parenchyma and perivascular spaces of CSD brains. To further characterize the impact of stress on the cerebrovasculature, brain endothelial cells (bECs) were isolated, and global gene expression profiles were generated. Bioinformatic analysis of CSD-induced transcriptional changes in bECs showed enrichment in pathways that delineate the vascular response to injury. These pathways followed a temporal sequence of inflammation, oxidative stress, growth factor signaling, and wound healing (i.e., platelet aggregation, hemostasis, fibrinogen deposition, and angiogenesis). Immunohistochemical staining for markers of fibrinogen deposition and angiogenesis confirmed the existence of the markers at the sites of vascular disruptions. Recovery after CSD cessation was marked by recruitment of leukocytes perhaps participating in vascular repair. The data suggest that co-morbidity of affective disorders and vascular diseases may be attributed in part to a common link in altered endothelial cell function.

Indexed as

Social DefeatAnimalsBlood-Brain BarrierBrainEndothelial CellsMaleMiceMice, Inbred C57BLStress, PsychologicalAngiogenesisBlood-brain barrierCerebrovasculatureDepressionEndotheliaFibrinogenInflammationLeukocyteNeuroimmunePsychosocial stress

Identifiers

PMID32413560
PMCPMC7416466
OpenAlexW3025540999

What OpenQuestion holds

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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.