Evidence map›Paper›PMID 28542131›Full record

ArticleCell death & disease2017

Aroclor1254 disrupts the blood-testis barrier by promoting endocytosis and degradation of junction proteins via p38 MAPK pathway.

Xiaoyu Jia, Ying Xu, Weixing Wu, Yunxia Fan, Guoli Wang, Tianbiao Zhang, Wenhui Su

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. 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
2.0field-weighted citation impact, top 12% 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, 74 citations in OpenAlex.

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  8. Transcription factorZoological research · 2023
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  14. Review
  15. Role of p38 MAPK Signalling in Testis Development and Male Fertility.Oxidative medicine and cellular longevity · 2022
    Review
  16. Article
  17. The Roles of Junctional Adhesion Molecules (JAMs) in Cell Migration.Frontiers in cell and developmental biology · 2022
    Review
  18. Article
  19. Article
  20. UropathogenicFrontiers in immunology · 2021
    Article
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.

Xiaoyu JiaDepartment of Biochemistry and Molecular Biology, College of Basic Medical Science, China Medical University, Shenyang 110001, China.
Ying XuDepartment of Biochemistry and Molecular Biology, College of Basic Medical Science, China Medical University, Shenyang 110001, China.
Weixing WuDepartment of Biochemistry and Molecular Biology, College of Basic Medical Science, China Medical University, Shenyang 110001, China.
Yunxia FanDepartment of Biochemistry and Molecular Biology, College of Basic Medical Science, China Medical University, Shenyang 110001, China.
Guoli WangDepartment of Biochemistry and Molecular Biology, College of Basic Medical Science, China Medical University, Shenyang 110001, China.
Tianbiao ZhangDepartment of Biochemistry and Molecular Biology, College of Basic Medical Science, China Medical University, Shenyang 110001, China.
Wenhui SuDepartment of Biochemistry and Molecular Biology, College of Basic Medical Science, China Medical University, Shenyang 110001, China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The blood-testis barrier (BTB) constituted by coexisting junction apparatus between Sertoli cells (SCs) plays an important role in spermatogenesis, which is a known target of various environmental toxicants. The commercial polychlorinated biphenyls mixture, Aroclor1254, has been shown to impair male reproduction by decreasing sperm count and affecting SC metabolism. This study was designed to investigate the effects of Aroclor1254 on the BTB integrity and elucidate the underlying mechanisms. We found that Aroclor1254 treatment in rats (1 or 3 mg/kg per day for 21 consecutive days) and in primary cultured SCs (5 or 10 μg/ml for 48 h) could induce BTB disruption via p38 MAPK pathway, concurrently with increments in junction proteins (JAM-A, N-cadherin, and β-catenin) endocytosis, and occludin ubiquitination. Either inhibition of caveolin-dependent membrane protein internalization by cholesterol oxidase or silencing E3 ubiquitine ligase Itch by small interfering RNA could partially counteract the effects of Aroclor1254 on the barrier function of cultured SCs. These results demonstrate that Aroclor1254 disrupts the BTB function by promoting the caveolin-dependent endocytosis and ubiquitine-proteasome degradation of junction proteins through the p38 MAPK pathway, which might be the potential reasons for its negative effects on spermatogenesis and male reproduction.

Indexed as

AnimalsBlood-Testis BarrierCells, CulturedChlorodiphenyl (54% Chlorine)EndocytosisEpitheliumGene Knockdown TechniquesMaleMAP Kinase Signaling SystemOccludinp38 Mitogen-Activated Protein KinasesProteolysisRats, Sprague-DawleySertoli CellsTight Junction ProteinsUbiquitinationChlorodiphenyl (54% Chlorine)Itch protein, ratOccludinp38 Mitogen-Activated Protein KinasesTight Junction ProteinsUbiquitin-Protein Ligases

Identifiers

PMID28542131
PMCPMC5520738
OpenAlexW2620065941

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.