Evidence map›Paper›PMID 21697081›Full record

ArticleThe Journal of biological chemistry2011

Monoamine oxidase a expression is vital for embryonic brain development by modulating developmental apoptosis.

Chi Chiu Wang, Astrid Borchert, Aslihan Ugun-Klusek, Ling Yin Tang, Wai Ting Lui, Ching Yan Chu, Ellen Billett, Hartmut Kuhn, Christoph Ufer

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Type A monoamine oxidase; its unique role in mood, behavior and neurodegeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2025
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  16. 90 years of monoamine oxidase: some progress and some confusion.Journal of neural transmission (Vienna, Austria : 1996) · 2018
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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

9 authors at 3 institutions in 3 countries.

Chi Chiu WangInstitute of Biochemistry, University Medicine Berlin-Charité, Oudenarder Strasse 16, 13347 Berlin, Germany.
Astrid Borchert
Aslihan Ugun-Klusek
Ling Yin Tang
Wai Ting Lui
Ching Yan Chu
Ellen Billett
Hartmut Kuhn
Christoph Ufer
Chinese University of Hong Kong · CNNottingham Trent University · GBCharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Monoamine oxidases (MAO-A, MAO-B) metabolize biogenic amines and have been implicated in neuronal apoptosis. Although apoptosis is an important process in embryo development, the role of MAO isoenzymes has not been investigated in detail. We found that expression of MAO-A and MAO-B can be detected early on during embryo development. Expression levels remained constant until around midgestation but then dropped to almost undetectable levels toward birth. Similar expression kinetics were observed in the brain. Isoform-specific expression silencing of MAO-A mediated by siRNA during in vitro embryogenesis induced developmental defects, as indicated by a reduction of the crown rump length and impaired cerebral development. These alterations were paralleled by elevated serotonin levels. Similar abnormalities were observed when embryos were cultured in the presence of the MAO-A inhibitor clorgyline or when the transcriptional inhibitor of MAO-A expression R1 was overexpressed. In contrast, no such alterations were detected when expression of MAO-B was knocked down. To explore the underlying mechanisms for the developmental abnormalities in MAO-A knockdown embryos, we quantified the degree of developmental apoptosis in the developing brain. MAO-A knockdown reduced the number of apoptotic cells in the neuroepithelium, which coincided with impaired activation of caspases 3 and 9. Moreover, we observed reduced cyclin D1 levels as an indicator of impaired cell proliferation in MAO-A knockdown embryos. This data highlights MAO-A as a vital regulator of embryonic brain development.

Indexed as

BrainEmbryo, MammalianAnimalsApoptosisCaspase 3Caspase 9Cell ProliferationClorgylineCyclin D1Gene Expression Regulation, DevelopmentalGene Expression Regulation, EnzymologicGene Knockdown TechniquesMiceMonoamine OxidaseMonoamine Oxidase InhibitorsRNA, Small InterferingCasp3 protein, mouseCasp9 protein, mouseCaspase 3Caspase 9Ccnd1 protein, mouseClorgylineCyclin D1Monoamine OxidaseMonoamine Oxidase InhibitorsRNA, Small Interfering

Identifiers

PMID21697081
PMCPMC3151076
OpenAlexW2097906078

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.