Evidence map›Paper›PMID 29572511›Full record

ArticleScientific reports2018

Double deletion of tetraspanins CD9 and CD81 in mice leads to a syndrome resembling accelerated aging.

Yingji Jin, Yoshito Takeda, Yasushi Kondo, Lokesh P Tripathi, Sujin Kang, Hikari Takeshita, Hanako Kuhara, Yohei Maeda, Masayoshi Higashiguchi, Kotaro Miyake and 24 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. CD81eLife · 2025
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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

34 authors at 3 institutions in 1 country.

Yingji JinDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Yoshito TakedaDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan. yoshito@imed3.med.osaka-u.ac.jp.
Yasushi KondoSumitomo Dainippon Pharma Co., Ltd, Osaka, Japan.
Lokesh P TripathiNational Institute of Biomedical Innovation, Health and Nutrition, Ibaraki, Osaka, Japan.
Sujin KangDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Hikari TakeshitaDepartment of Geriatric Medicine &, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Hanako KuharaDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Yohei MaedaDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Masayoshi HigashiguchiDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Kotaro MiyakeDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Osamu MorimuraDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Taro KobaDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Yoshitomo HayamaDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Shohei KoyamaDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Kaori NakanishiDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Takeo IwasakiDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Satoshi TetsumotoDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Kazuyuki TsujinoDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Muneyoshi KuroyamaDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Kota IwahoriDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Haruhiko HirataDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Takayuki TakimotoDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Mayumi SuzukiDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Izumi NagatomoDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Ken SugimotoDepartment of Geriatric Medicine &, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Yuta FujiiSumitomo Dainippon Pharma Co., Ltd, Osaka, Japan.
Hiroshi KidaDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Kenji MizuguchiNational Institute of Biomedical Innovation, Health and Nutrition, Ibaraki, Osaka, Japan.ORCID 0000-0003-3021-7078
Mari ItoNational Institute of Biomedical Innovation, Health and Nutrition, Ibaraki, Osaka, Japan.
Takashi KijimaDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Hiromi RakugiDepartment of Geriatric Medicine &, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.ORCID 0000-0001-6508-4338
Eisuke MekadaDepartment of Cell Biology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
Isao TachibanaDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Atsushi KumanogohDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
The University of Osaka · JPNational Institute of Biomedical Innovation, Health and Nutrition · JPSumitomo Dainippon Pharma (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) has been recently characterized as a disease of accelerated lung aging, but the mechanism remains unclear. Tetraspanins have emerged as key players in malignancy and inflammatory diseases. Here, we found that CD9/CD81 double knockout (DKO) mice with a COPD-like phenotype progressively developed a syndrome resembling human aging, including cataracts, hair loss, and atrophy of various organs, including thymus, muscle, and testis, resulting in shorter survival than wild-type (WT) mice. Consistent with this, DNA microarray analysis of DKO mouse lungs revealed differential expression of genes involved in cell death, inflammation, and the sirtuin-1 (SIRT1) pathway. Accordingly, expression of SIRT1 was reduced in DKO mouse lungs. Importantly, siRNA knockdown of CD9 and CD81 in lung epithelial cells additively decreased SIRT1 and Foxo3a expression, but reciprocally upregulated the expression of p21 and p53, leading to reduced cell proliferation and elevated apoptosis. Furthermore, deletion of these tetraspanins increased the expression of pro-inflammatory genes and IL-8. Hence, CD9 and CD81 might coordinately prevent senescence and inflammation, partly by maintaining SIRT1 expression. Altogether, CD9/CD81 DKO mice represent a novel model for both COPD and accelerated senescence.

Indexed as

Aging, PrematureLungPulmonary Disease, Chronic ObstructiveAnimalsDisease Models, AnimalForkhead Box Protein O3Gene Expression RegulationHumansMiceMice, KnockoutRespiratory MucosaSirtuin 1SyndromeTetraspanin 28Tetraspanin 29Tumor Suppressor Protein p53Cd81 protein, mouseCd9 protein, mouseForkhead Box Protein O3FoxO3 protein, mouseSirt1 protein, mouseSirtuin 1Tetraspanin 28Tetraspanin 29Trp53 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID29572511
PMCPMC5865149
OpenAlexW2806239152

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.