Evidence map›Paper›PMID 18830269›Full record

ArticleThe Journal of investigative dermatology2009

Auf1/Hnrnpd-deficient mice develop pruritic inflammatory skin disease.

Navid Sadri, Robert J Schneider

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.5field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
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  4. Article
  5. Article
  6. Review
  7. Post-transcriptional checkpoints in autoimmunity.Nature reviews. Rheumatology · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. RNA metabolism and links to inflammatory regulation and disease.Cellular and molecular life sciences : CMLS · 2021
    Review
  13. Review
  14. The trans-omics landscape of COVID-19.Nature communications · 2021
    Article
  15. Differential modulation of Ahr and Arid5a: A promising therapeutic strategy for autoimmune encephalomyelitis.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2020
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Navid SadriDepartment of Microbiology, New York University School of Medicine, New York, New York 10003, USA.
Robert J Schneider
New York University · US

Funding

INFECTIOUS DISEASES &BASIC MICROBIOLOGICAL MECHANISMST32AI007180 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WEISER, JEFFREY NEAL · 1985 to 2022
$8.9M
Control of Cytoxine mRNA Stability by AUF1R01GM060428 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SCHNEIDER, ROBERT · 2000 to 2007
$2.4M
Ionizing Radiation Control of Inflammatory Cytokine mRNA Stability and ExpressionR01GM085693 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SCHNEIDER, ROBERT JAY · 2009 to 2013
$1.7M
LEICA TCS SP2 ADBS CONFOCAL MICROSCOPES10RR017970 · NCRR · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BOROWIEC, JAMES A. · 2003 to 2003
$361k
NCRR NIH HHS S10 RR017970NIAID NIH HHS T32 AI007180NIGMS NIH HHS R01 GM060428NIGMS NIH HHS R01 GM085693
6 · The paper itself

Abstract

Mice lacking heterogenous nuclear ribonuclear protein D (Hnrnpd), also known as Auf1, a regulator of inflammatory cytokine mRNA stability, develop chronic dermatitis with age that is characterized by pruritus and excoriations. Histological analysis showed marked epidermal acanthosis and spongiosis, neovascularization, and elevated number of inflammatory cells, including T cells, macrophages, neutrophils, mast cells, and eosinophils. Hnrnpd-deficient (Hnrnpd(tm1Rjsc)) mice with dermatitis display elevated serum IgE levels. Lesions in Hnrnpd(tm1Rjsc) mice were associated with a shift towards a Th(2) immune environment. Evaluation of T-cell-mediated skin inflammation by assaying contact hypersensitivity indicated an increased response in Hnrnpd(tm1Rjsc) mice. T cells and macrophages from Hnrnpd(tm1Rjsc) mice demonstrate a number of abnormalities associated with dermatitis, including increased IL2, tumor-necrosis factor-alpha (TNFalpha), and IL1beta production. Finally, many features of spontaneous dermatitis could be recapitulated in experimentally induced lesions by subcutaneous injection of CCL27 and TNF in unaffected Hnrnpd(tm1Rjsc) mice. Collectively, these data highlight the importance of HNRNPD and proper regulation of mRNA stability in the intricate processes of leukocyte recruitment and inflammatory activation within the skin.

Indexed as

AnimalsChemokine CCL27CytokinesDermatitisFemaleHeterogeneous-Nuclear Ribonucleoprotein DHeterogeneous Nuclear Ribonucleoprotein D0InflammationInterleukin-1betaInterleukin-2MacrophagesMaleMicep38 Mitogen-Activated Protein KinasesPruritusTumor Necrosis Factor-alphaCCL27 protein, humanChemokine CCL27CytokinesHeterogeneous-Nuclear Ribonucleoprotein DHeterogeneous Nuclear Ribonucleoprotein D0HNRNPD protein, humanHnrpd protein, mouseInterleukin-1betaInterleukin-2p38 Mitogen-Activated Protein KinasesTumor Necrosis Factor-alpha

Identifiers

PMID18830269
PMCPMC4074411
OpenAlexW1986521568

What OpenQuestion holds

Textmetadata
LicenceTDM
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.