Evidence map›Paper›PMID 36982275›Full record

ArticleInternational journal of molecular sciences2023

The Antimicrobial Peptide AMP-IBP5 Suppresses Dermatitis-like Lesions in a Mouse Model of Atopic Dermatitis through the Low-Density Lipoprotein Receptor-Related Protein-1 Receptor.

Hai Le Thanh Nguyen, Ge Peng, Juan Valentin Trujillo-Paez, Hainan Yue, Risa Ikutama, Miho Takahashi, Yoshie Umehara, Ko Okumura, Hideoki Ogawa, Shigaku Ikeda and 1 more

Open access · goldFull text 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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Antimicrobial Peptide Signaling in Skin Diseases.JID innovations : skin science from molecules to population health · 2025
    Review
  6. Article
  7. Review
  8. Review
  9. Are Antimicrobial Peptides a 21st-Century Solution for Atopic Dermatitis?International journal of molecular sciences · 2023
    Review
  10. Editorial of Special Issue "Molecular Mechanisms of Allergy and Asthma 2.0".International journal of molecular sciences · 2023
    Article
  11. 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

11 authors at 1 institution in 1 country.

Hai Le Thanh NguyenAtopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan.ORCID 0000-0002-9566-2458
Ge PengAtopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan.ORCID 0000-0002-3278-2604
Juan Valentin Trujillo-PaezAtopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan.
Hainan YueAtopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan.
Risa IkutamaAtopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan.
Miho TakahashiAtopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan.
Yoshie UmeharaAtopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan.
Ko OkumuraAtopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan.
Hideoki OgawaAtopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan.
Shigaku IkedaAtopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan.
François NiyonsabaAtopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan.ORCID 0000-0002-0588-8315
Juntendo University · JP

Funding

Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology, Japan 21K08309Juntendo University 2021-38National Eczema Association Research Grant NEA21-ERG159
6 · The paper itself

Abstract

The antimicrobial peptide derived from insulin-like growth factor-binding protein 5 (AMP-IBP5) exhibits antimicrobial activities and immunomodulatory functions in keratinocytes and fibroblasts. However, its role in regulating skin barrier function remains unclear. Here, we investigated the effects of AMP-IBP5 on the skin barrier and its role in the pathogenesis of atopic dermatitis (AD). 2,4-Dinitrochlorobenzene was used to induce AD-like skin inflammation. Transepithelial electrical resistance and permeability assays were used to investigate tight junction (TJ) barrier function in normal human epidermal keratinocytes and mice. AMP-IBP5 increased the expression of TJ-related proteins and their distribution along the intercellular borders. AMP-IBP5 also improved TJ barrier function through activation of the atypical protein kinase C and Rac1 pathways. In AD mice, AMP-IBP5 ameliorated dermatitis-like symptoms restored the expression of TJ-related proteins, suppressed the expression of inflammatory and pruritic cytokines, and improved skin barrier function. Interestingly, the ability of AMP-IBP5 to alleviate inflammation and improve skin barrier function in AD mice was abolished in mice treated with an antagonist of the low-density lipoprotein receptor-related protein-1 (LRP1) receptor. Collectively, these findings indicate that AMP-IBP5 may ameliorate AD-like inflammation and enhance skin barrier function through LRP1, suggesting a possible role for AMP-IBP5 in the treatment of AD.

Indexed as

Dermatitis, AtopicAnimalsAntimicrobial PeptidesCytokinesDisease Models, AnimalHumansInflammationKeratinocytesLipoproteins, LDLMiceSkinAntimicrobial PeptidesCytokinesLipoproteins, LDLAMP-IBP5antimicrobial peptideatopic dermatitisbarrier functionskin barrier

Identifiers

PMID36982275
PMCPMC10049508
OpenAlexW4323665116

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read40
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.