Evidence map›Paper›PMID 26046540›Full record

ArticlePloS one2015

Downregulation of TNIP1 Expression Leads to Increased Proliferation of Human Keratinocytes and Severer Psoriasis-Like Conditions in an Imiquimod-Induced Mouse Model of Dermatitis.

Yan Chen, Heng Yan, Zhiqiang Song, Fangru Chen, Huan Wang, Jun Niu, Xiaowei Shi, Dongmei Zhang, Na Zhang, Zhifang Zhai and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Repressive Control of Keratinocyte Cytoplasmic Inflammatory Signaling.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. TNIP1 RegulatesFrontiers in immunology · 2018
    Article
  16. Review
  17. Article
  18. 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

14 authors at 2 institutions in 1 country.

Yan ChenDepartment of Dermatology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Heng YanDepartment of Dermatology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Zhiqiang SongDepartment of Dermatology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Fangru ChenDepartment of Dermatology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Huan WangDepartment of Dermatology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Jun NiuDepartment of Dermatology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Xiaowei ShiDepartment of Dermatology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Dongmei ZhangDepartment of Dermatology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Na ZhangDepartment of Dermatology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Zhifang ZhaiDepartment of Dermatology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Baiyu ZhongDepartment of Dermatology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Liangjin ChengDepartment of Dermatology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Tian QianDepartment of Dermatology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Fei HaoDepartment of Dermatology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Southwest Hospital · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is a chronic, inflammatory skin disease involving both environmental and genetic factors. According to genome-wide association studies (GWAS), the TNIP1 gene, which encodes the TNF-α-induced protein 3-interacting protein 1 (TNIP1), is strongly linked to the susceptibility of psoriasis. TNIP1 is a widely expressed ubiquitin sensor that binds to the ubiquitin-editing protein A20 and restricts TNF- and TLR-induced signals. In our study, TNIP1 expression decreased in specimens of epidermis affected by psoriasis. Based on previous studies suggesting a role for TNIP1 in modulating cancer cell growth, we investigated its role in keratinocyte proliferation, which is clearly abnormal in psoriasis. To mimic the downregulation or upregulation of TNIP1 in HaCaT cells and primary human keratinocytes (PHKs), we used a TNIP1 specific small interfering hairpin RNA (TNIP1 shRNA) lentiviral vector or a recombinant TNIP1 (rTNIP1) lentiviral vector, respectively. Blocking TNIP1 expression increased keratinocyte proliferation, while overexpression of TNIP1 decreased keratinocyte proliferation. Furthermore, we showed that TNIP1 signaling might involve extracellular signal-regulated kinase1/2 (Erk1/2) and CCAAT/enhancer-binding protein β (C/EBPβ) activity. Intradermal injection of TNIP1 shRNA in BALB/c mice led to exaggerated psoriatic conditions in imiquimod (IMQ)-induced psoriasis-like dermatitis. These findings indicate that TNIP1 has a protective role in psoriasis and therefore could be a promising therapeutic target.

Indexed as

AminoquinolinesAnimalsCCAAT-Enhancer-Binding Protein-betaCell ProliferationCells, CulturedDermatitisDisease Models, AnimalDNA-Binding ProteinsDown-RegulationHumansImiquimodKeratinocytesMiceMice, Inbred BALB CMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3AminoquinolinesCCAAT-Enhancer-Binding Protein-betaDNA-Binding ProteinsImiquimodMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3TNIP1 protein, human

Identifiers

PMID26046540
PMCPMC4457880
OpenAlexW1955733588

What OpenQuestion holds

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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.