Evidence map›Paper›PMID 30402708›Full record

ArticleMolecular neurobiology2019

Prenatal Exposure to Benzophenone-3 Impairs Autophagy, Disrupts RXRs/PPARγ Signaling, and Alters Epigenetic and Post-Translational Statuses in Brain Neurons.

Agnieszka Wnuk, Joanna Rzemieniec, Jakub Staroń, Ewa Litwa, Władysław Lasoń, Andrzej Bojarski, Małgorzata Kajta

Open access · hybridAbstract read
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Agnieszka WnukInstitute of Pharmacology, Department of Experimental Neuroendocrinology, Laboratory of Molecular Neuroendocrinology, Polish Academy of Sciences, Smetna Street 12, 31-343, Krakow, Poland.
Joanna RzemieniecInstitute of Pharmacology, Department of Experimental Neuroendocrinology, Laboratory of Molecular Neuroendocrinology, Polish Academy of Sciences, Smetna Street 12, 31-343, Krakow, Poland.
Jakub StarońInstitute of Pharmacology, Department of Medicinal Chemistry, Polish Academy of Sciences, Smetna Street 12, 31-343, Krakow, Poland.
Ewa LitwaInstitute of Pharmacology, Department of Experimental Neuroendocrinology, Polish Academy of Sciences, Smetna Street 12, 31-343, Krakow, Poland.
Władysław LasońInstitute of Pharmacology, Department of Experimental Neuroendocrinology, Polish Academy of Sciences, Smetna Street 12, 31-343, Krakow, Poland.
Andrzej BojarskiInstitute of Pharmacology, Department of Medicinal Chemistry, Polish Academy of Sciences, Smetna Street 12, 31-343, Krakow, Poland.
Małgorzata KajtaInstitute of Pharmacology, Department of Experimental Neuroendocrinology, Laboratory of Molecular Neuroendocrinology, Polish Academy of Sciences, Smetna Street 12, 31-343, Krakow, Poland. kajta@if-pan.krakow.pl.ORCID http://orcid.org/0000-0003-0616-7031
Maj Institute of Pharmacology · PL

Funding

National Science Centre of Poland 2014/13/N/NZ4/04845
6 · The paper itself

Abstract

The UV absorber benzophenone-3 (BP-3) is the most extensively used chemical substance in various personal care products. Despite that BP-3 exposure is widespread, knowledge about the impact of BP-3 on the brain development is negligible. The present study aimed to explore the mechanisms of prenatal exposure to BP-3 in neuronal cells, with particular emphasis on autophagy and nuclear receptors signaling as well as the epigenetic and post-translational modifications occurring in response to BP-3. To observe the impact of prenatal exposure to BP-3, we administered BP-3 to pregnant mice, and next, we isolated brain tissue from pretreated embryos for primary cell neocortical culture. Our study revealed that prenatal exposure to BP-3 (used in environmentally relevant doses) impairs autophagy in terms of BECLIN-1, MAP1LC3B, autophagosomes, and autophagy-related factors; disrupts the levels of retinoid X receptors (RXRs) and peroxisome proliferator-activated receptor gamma (PPARγ); alters epigenetic status (i.e., attenuates HDAC and sirtuin activities); inhibits post-translational modifications in terms of global sumoylation; and dysregulates expression of neurogenesis- and neurotransmitter-related genes as well as miRNAs involved in pathologies of the nervous system. Our study also showed that BP-3 has good permeability through the BBB. We strongly suggest that BP-3-evoked effects may substantiate a fetal basis of the adult onset of neurological diseases, particularly schizophrenia and Alzheimer's disease.

Indexed as

Epigenesis, GeneticAnimalsAutophagosomesAutophagyBenzophenonesBlood-Brain BarrierBrainEmbryo, MammalianFemaleHistone AcetyltransferasesHistone DeacetylasesMiceMicroRNAsNeurogenesisNeuronsNeurotransmitter AgentsBenzophenonesHistone AcetyltransferasesHistone DeacetylasesMicroRNAsNeurotransmitter AgentsoxybenzonePPAR gammaRetinoid X ReceptorsRNA, MessengerSirtuinsAutophagyBenzophenone-3BP-3miRNANeuronal cellPrenatal exposure

Identifiers

PMID30402708
PMCPMC6647400
OpenAlexW2899762839

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.