Evidence map›Paper›PMID 29861095›Full record

ArticleBiological psychiatry2018

Connective Tissue Growth Factor Is a Novel Prodepressant.

Cortney A Turner, Vikram Sharma, Megan H Hagenauer, Sraboni Chaudhury, Angela M O'Connor, Elaine K Hebda-Bauer, Robert C Thompson, Richard M Myers, William E Bunney, Jack D Barchas and 4 more

Abstract read
In one paragraph

Article in Biological psychiatry, 2018. 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
1.7field-weighted citation impact, top 16% 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, 27 citations in OpenAlex.

  1. Elevated reactive aggression in forebrain-specificJournal of cell communication and signaling · 2024
    Article
  2. A Prelimbic Cortex-Thalamus Circuit Bidirectionally Regulates Innate and Stress-Induced Anxiety-Like Behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
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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

14 authors at 5 institutions in 1 country.

Cortney A TurnerMolecular & Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, Michigan. Electronic address: caturner@umich.edu.
Vikram SharmaMolecular & Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, Michigan.
Megan H HagenauerMolecular & Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, Michigan.
Sraboni ChaudhuryMolecular & Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, Michigan.
Angela M O'ConnorMolecular & Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, Michigan.
Elaine K Hebda-BauerMolecular & Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, Michigan.
Robert C ThompsonMolecular & Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, Michigan; Department of Psychiatry, University of Michigan, Ann Arbor, Michigan.
Richard M MyersHudsonAlpha Institute for Biotechnology, Huntsville, Alabama.
William E BunneyPsychiatry & Human Behavior, University of California, Irvine, Irvine.
Jack D BarchasDepartment of Psychiatry, Weill Cornell Medical College, New York, New York.
Francis S LeeDepartment of Psychiatry, Weill Cornell Medical College, New York, New York.
Alan F SchatzbergDepartment of Psychiatry & Behavioral Sciences, Stanford University, Palo Alto, California.
Stanley J WatsonMolecular & Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, Michigan; Department of Psychiatry, University of Michigan, Ann Arbor, Michigan.
Huda AkilMolecular & Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, Michigan; Department of Psychiatry, University of Michigan, Ann Arbor, Michigan.
University of Michigan–Ann Arbor · USCornell University · USHudsonAlpha Institute for Biotechnology · USStanford University · USUniversity of California, Irvine · US

Funding

Project 5: High-Throughput Analysis of Gene RegulationP50MH060398 · NIMH · UNIVERSITY OF CALIFORNIA-IRVINE · PI BUNNEY, WILLIAM E · 1999 to 2008
$12.7M
Investigating the role of Bmp4 in glial subtype specification and temperamentU01DA043098 · NIDA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HUDA AKIL, Jun Li · 2017 to 2026
$6.9M
Can Affective Resilience be Enhanced? A Developmental and Epigenetic ApproachR01MH104261 · NIMH · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI AKIL, HUDA, WATSON, STANLEY J · 2014 to 2018
$2.8M
NIDA NIH HHS U01 DA043098NIMH NIH HHS P50 MH060398NIMH NIH HHS R01 MH104261
6 · The paper itself

Abstract

backgroundWhile downregulation of several growth factors in major depressive disorder is well established, less attention has been paid to the upregulation of other growth factors. Yet, upregulated growth factors may offer better therapeutic targets. We show that connective tissue growth factor (CTGF) represents a target based on its upregulation in major depressive disorder and studies in animal models implicating it in negative affect.

methodsCTGF gene expression was first evaluated in the postmortem human amygdala. The findings were followed up in outbred rats and in two rat lines that were selectively bred for differences in novelty-seeking and anxiety behavior (bred low responders and bred high responders). We studied the impact of social defeat and early-life treatment with fibroblast growth factor 2 on CTGF expression. Finally, we assessed the ability of an anti-CTGF antibody (FG-3019) to alter CTGF expression and emotionality.

resultsIn the human amygdala, CTGF expression was significantly increased in major depressive disorder compared with control subjects. CTGF expression was also significantly increased in the dentate gyrus of adult bred low responders compared with bred high responders. Social defeat stress in bred low responders significantly increased CTGF expression in the dentate gyrus. Early-life fibroblast growth factor 2, a treatment that reduces anxiety-like behavior throughout life, decreased CTGF expression in the adult dentate gyrus. In outbred rats, CTGF administration increased depression-like behavior. Chronic treatment with FG-3019 decreased CTGF expression, and acute and chronic treatment was antidepressant.

conclusionsThis study is the first to implicate CTGF as a prodepressant molecule that could serve as a target for the development of novel therapeutics.

Indexed as

AdultAmygdalaAnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAnxietyConnective Tissue Growth FactorDentate GyrusDisease Models, AnimalExploratory BehaviorFemaleFibroblast Growth Factor 2Gene Expression ProfilingHippocampusHumansMajor Depressive DisorderAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedCCN2 protein, humanConnective Tissue Growth FactorFibroblast Growth Factor 2pamrevlumabAmygdalaDentate gyrusDepressionFGF2HippocampusStress

Identifiers

PMID29861095
PMCPMC6249676
OpenAlexW2799447218

What OpenQuestion holds

Textmetadata
LicenceTDM
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.