Evidence map›Paper›PMID 37446281›Full record

ArticleInternational journal of molecular sciences2023

Increased Interleukin-36β Expression Promotes Angiogenesis in Japanese Atopic Dermatitis.

Reo Komaki, Tomomitsu Miyagaki, Miho Tanaka, Kaori Nakajima, Tatsuro Okano, Sora Takeuchi, Takafumi Kadono

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. 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.

Reo KomakiDepartment of Dermatology, St. Marianna University School of Medicine, Kawasaki 216-8511, Japan.
Tomomitsu MiyagakiDepartment of Dermatology, St. Marianna University School of Medicine, Kawasaki 216-8511, Japan.ORCID 0000-0003-1879-3128
Miho TanakaDepartment of Dermatology, St. Marianna University School of Medicine, Kawasaki 216-8511, Japan.
Kaori NakajimaDepartment of Dermatology, St. Marianna University School of Medicine, Kawasaki 216-8511, Japan.
Tatsuro OkanoDepartment of Dermatology, St. Marianna University School of Medicine, Kawasaki 216-8511, Japan.
Sora TakeuchiDepartment of Dermatology, St. Marianna University School of Medicine, Kawasaki 216-8511, Japan.
Takafumi KadonoDepartment of Dermatology, St. Marianna University School of Medicine, Kawasaki 216-8511, Japan.
St. Marianna University School of Medicine · JP

Funding

Ministry of Education, Culture, Sports, Science and Technology 16K19709Ministry of Education, Culture, Sports, Science and Technology 23K07797
6 · The paper itself

Abstract

While atopic dermatitis (AD) is considered as a T helper 2 (Th2)-centered disease, an increase in other types of inflammatory cytokines is also noted in AD and they may also contribute to the development of the disease. Recently, the efficacy of an anti-IL-36 receptor antibody in AD was demonstrated in a clinical trial. Although there have been several reports on IL-36α and IL-36γ expression and function in AD, IL-36β has been barely studied. In this report, we examined IL-36β expression and function using clinical samples of AD and the epidermal keratinocyte cell line, HaCaT cells. We demonstrated that IL-36β expression in epidermal keratinocytes was increased in AD lesional skin compared to healthy skin. IL-36β promoted vascular endothelial growth factor A production in HaCaT keratinocytes through phosphorylation of extracellular signal-regulated kinases 1 and 2. In addition, IL-36β up-regulated placental growth factor mRNA expression in HaCaT keratinocytes. IL-36β expression levels in epidermal keratinocytes were correlated with the number of dermal vessels in AD skin. These results suggest that IL-36β may play an important role for angiogenesis in lesional skin of AD and that IL-36β can be a therapeutic target in AD.

Indexed as

Dermatitis, AtopicInterleukin-1East Asian PeopleHaCaT CellsHumansKeratinocytesPlacenta Growth FactorVascular Endothelial Growth Factor AIL36B protein, humanInterleukin-1Placenta Growth FactorVascular Endothelial Growth Factor AangiogenesisAsian populationatopic dermatitisIL-36βvascular endothelial growth factor A

Identifiers

PMID37446281
PMCPMC10341928
OpenAlexW4383376443

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.