Evidence map›Paper›PMID 25502632›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2015

Evidence revealing deregulation of the KLF11-MAO A pathway in association with chronic stress and depressive disorders.

Sharonda Harris, Shakevia Johnson, Jeremy W Duncan, Chinelo Udemgba, Jeffrey H Meyer, Paul R Albert, Gwen Lomberk, Raul Urrutia, Xiao-Ming Ou, Craig A Stockmeier and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. Frontiers in nutrition · 2026
    Review
  2. Type A monoamine oxidase; its unique role in mood, behavior and neurodegeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2025
    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 5 institutions in 2 countries.

Sharonda HarrisDepartment of Psychiatry and Human Behavior, Jackson, MS, USA.
Shakevia JohnsonDepartment of Psychiatry and Human Behavior, Jackson, MS, USA.
Jeremy W Duncan1] Department of Psychiatry and Human Behavior, Jackson, MS, USA [2] Program in Neuroscience, Jackson, MS, USA.
Chinelo UdemgbaDepartment of Psychiatry and Human Behavior, Jackson, MS, USA.
Jeffrey H MeyerCentre for Addiction and Mental Health and Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada.
Paul R AlbertOttawa Hospital Research Institute (Neuroscience), Ottawa, Ontario, Canada.
Gwen LomberkEpigenetics and Chromatin Dynamics Laboratory, GI Research Unit, Mayo Clinic, Rochester, MN, USA.
Raul UrrutiaEpigenetics and Chromatin Dynamics Laboratory, GI Research Unit, Mayo Clinic, Rochester, MN, USA.
Xiao-Ming OuDepartment of Psychiatry and Human Behavior, Jackson, MS, USA.
Craig A Stockmeier1] Department of Psychiatry and Human Behavior, Jackson, MS, USA [2] Department of Psychiatry, Case Western Reserve University, Cleveland, OH, USA.
Jun Ming Wang1] Department of Psychiatry and Human Behavior, Jackson, MS, USA [2] Program in Neuroscience, Jackson, MS, USA [3] Department of Pathology, University of Mississippi Medical Center, Jackson, MS, USA.
Mayo Clinic · USCase Western Reserve University · USCentre for Addiction and Mental Health · CAJackson Memorial Hospital · USOttawa Hospital · CA

Funding

Center for Psychiatric NeuroscienceP30GM103328 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI STOCKMEIER, CRAIG ALLEN · 2013 to 2017
$5.5M
Ethanol induced brain injury is decreased by inhibiting TIEG2 mediated cell deathR01AA020103 · NIAAA · UNIVERSITY OF MISSISSIPPI MED CTR · PI WANG, JUNMING · 2011 to 2014
$1.4M
Postmortem Human Brain Collection (Supplement to MH67996)R01MH067996 · NIMH · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI STOCKMEIER, CRAIG ALLEN · 2004 to 2007
$1.2M
CIHR 115098-1CIHR 123426-1NIAAA NIH HHS AA020103NIAAA NIH HHS R01 AA020103NIGMS NIH HHS P30 GM103328NIMH NIH HHS MH67996NIMH NIH HHS R01 MH067996
6 · The paper itself

Abstract

The biochemical pathways underlying major depressive disorder (MDD) and chronic stress are not well understood. However, it has been reported that monoamine oxidase A (MAO A, a major neurotransmitter-degrading enzyme) is significantly increased in the brains of human subjects affected with MDD and rats exposed to chronic social defeat (CSD) stress, which is used to model depression. In the current study, we compared the protein levels of a MAO A-transcriptional activator, Kruppel-like factor 11 (KLF11 , also recognized as transforming growth factor-beta-inducible early gene 2) between the brains of 18 human subjects with MDD and 18 control subjects. We found that, indeed, the expression of KLF11 is increased by 36% (p<0.02) in the postmortem prefrontal cortex of human subjects with MDD compared with controls. We also observed a positive correlation between KLF11 levels and those of its target gene, MAO A, both in association with MDD. KLF11 protein expression was also increased by 44% (p<0.02) in the frontal cortex of KLF11 wild-type mice (Klf11(+/+)) vs Klf11(-/-) when both exposed to CSD stress. In contrast, locomotor activities, central box duration and sucrose preference were significantly reduced in the stressed Klf11(+/+) mice, suggesting that Klf11(+/+) mice are more severely affected by the stress model compared with Klf11(-/-) mice. These results serve to assign an important role of KLF11 in upregulating MAO A in MDD and chronic social stress, suggesting that inhibition of the pathways regulated by this transcription factor may aid in the therapeutics of neuropsychiatric illnesses. Thus, the new knowledge derived from the current study extends our understanding of transcriptional mechanisms that are operational in the pathophysiology of common human diseases and thus bears significant biomedical relevance.

Indexed as

AnimalsApoptosis Regulatory ProteinsCell Cycle ProteinsChronic DiseaseDisease Models, AnimalDNA-Binding ProteinsDominance-SubordinationFemaleFrontal LobeHumansMajor Depressive DisorderMaleMice, Inbred C57BLMice, KnockoutMiddle AgedMonoamine OxidaseApoptosis Regulatory ProteinsCell Cycle ProteinsDNA-Binding ProteinsKLF11 protein, humanKLF11 protein, mouseMonoamine Oxidasemonoamine oxidase A, humanRepressor ProteinsTranscription Factors

Identifiers

PMID25502632
PMCPMC4397395
OpenAlexW2057337104

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.