Evidence map›Paper›PMID 27342862›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Dose-dependent role of claudin-1 in vivo in orchestrating features of atopic dermatitis.

Reitaro Tokumasu, Kosuke Yamaga, Yuji Yamazaki, Hiroyuki Murota, Koya Suzuki, Atsushi Tamura, Kana Bando, Yasuhide Furuta, Ichiro Katayama, Sachiko Tsukita

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

68 citing papers in PubMed, 131 citations in OpenAlex.

  1. Article
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  4. Protective Effect of Peony (Molecules (Basel, Switzerland) · 2025
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  12. Neutrophils in Atopic Dermatitis.Clinical reviews in allergy & immunology · 2024
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. International journal of molecular sciences · 2023
    Article

8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Reitaro TokumasuLaboratory of Biological Science, Graduate School of Frontier Biosciences and Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;
Kosuke YamagaLaboratory of Biological Science, Graduate School of Frontier Biosciences and Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan; Department of Dermatology, Course of integrated Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;
Yuji YamazakiLaboratory of Biological Science, Graduate School of Frontier Biosciences and Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan; Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544;
Hiroyuki MurotaDepartment of Dermatology, Course of integrated Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;
Koya SuzukiLaboratory of Biological Science, Graduate School of Frontier Biosciences and Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;
Atsushi TamuraLaboratory of Biological Science, Graduate School of Frontier Biosciences and Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;
Kana BandoLaboratory for Animal Resources and Genetic Engineering, RIKEN Center for Developmental Biology, 2-2-3 Minatojima Minami-machi, Chuou-ku, Kobe 650-0047, Japan.
Yasuhide FurutaLaboratory for Animal Resources and Genetic Engineering, RIKEN Center for Developmental Biology, 2-2-3 Minatojima Minami-machi, Chuou-ku, Kobe 650-0047, Japan.
Ichiro KatayamaDepartment of Dermatology, Course of integrated Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;
Sachiko TsukitaLaboratory of Biological Science, Graduate School of Frontier Biosciences and Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan; atsukita@biosci.med.osaka-u.ac.jp.
Osaka University · JPGenetic Resources Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease in humans. It was recently noted that the characteristics of epidermal barrier functions critically influence the pathological features of AD. Evidence suggests that claudin-1 (CLDN1), a major component of tight junctions (TJs) in the epidermis, plays a key role in human AD, but the mechanism underlying this role is poorly understood. One of the main challenges in studying CLDN1's effects is that Cldn1 knock-out mice cannot survive beyond 1 d after birth, due to lethal dehydration. Here, we established a series of mouse lines that express Cldn1 at various levels and used these mice to study Cldn1's effects in vivo. Notably, we discovered a dose-dependent effect of Cldn1's expression in orchestrating features of AD. In our experimental model, epithelial barrier functions and morphological changes in the skin varied exponentially with the decrease in Cldn1 expression level. At low Cldn1 expression levels, mice exhibited morphological features of AD and an innate immune response that included neutrophil and macrophage recruitment to the skin. These phenotypes were especially apparent in the infant stages and lessened as the mice became adults, depending on the expression level of Cldn1 Still, these adult mice with improved phenotypes showed an enhanced hapten-induced contact hypersensitivity response compared with WT mice. Furthermore, we revealed a relationship between macrophage recruitment and CLDN1 levels in human AD patients. Our findings collectively suggest that CLDN1 regulates the pathogenesis, severity, and natural course of human AD.

Indexed as

Disease Models, AnimalAdolescentAdultAgedAge FactorsAnimalsClaudin-1Dermatitis, AtopicEpidermisFemaleHumansMaleMiceMiddle AgedPermeabilityPhenotypeClaudin-1atopic dermatitisclaudin-1tight junctions

Identifiers

PMID27342862
PMCPMC4948351
OpenAlexW2469118718

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.