Evidence map›Paper›PMID 27239673›Full record

ArticleInflammation2016

PGRN Suppresses Inflammation and Promotes Autophagy in Keratinocytes Through the Wnt/β-Catenin Signaling Pathway.

Rong Tian, You Li, Xu Yao

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Dialogue between programmed cell death and psoriasis.Postepy dermatologii i alergologii · 2025
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Autophagy in the Neuronal Ceroid Lipofuscinoses (Batten Disease).Frontiers in cell and developmental biology · 2022
    Review
  18. Article
  19. Serum Progranulin As a Risk Predictor in Patients with Acute Myocardial Infarction.Medical science monitor : international medical journal of experimental and clinical research · 2021
    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

3 authors at 2 institutions in 1 country.

Rong TianDepartment of Dermatology, Air Force General Hospital of People's Liberation Army, Beijing, 100142, People's Republic of China. rongtianbs@163.com.
You LiDepartment of Dermatology, Air Force General Hospital of People's Liberation Army, Beijing, 100142, People's Republic of China.
Xu YaoDepartment of Dermatology, Air Force General Hospital of People's Liberation Army, Beijing, 100142, People's Republic of China. dryao_xu@126.com.
Air Force General Hospital PLA · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is a chronic, immune-mediated inflammatory skin disease that has a major impact on patients' quality of life. Progranulin (PGRN) is highly expressed in skin diseases and plays an important role in inflammation response and autophagy. However, the function of PGRN in the immune system and autophagy in psoriasis has not been clearly identified and elaborated on. Thus, this study aimed to investigate the role of PGRN on the inflammatory and autophagy process underlying inflammation in HaCaT cells. We showed that PGRN was markedly highly expressed in psoriasis lesions and inflammatory HaCaT cells. Specific silencing of PGRN promoted the production of the inflammatory cytokines IL-1β, IL-6, COX-2, iNOs, and MCP-1. Furthermore, PGRN siRNA promoted autophagy-related gene p62 and suppressed LC3II and Atg7 in HaCaT cells, while overexpression of PGRN showed a contrary effect. Moreover, knockdown of PGRN upregulated the expression levels of β-catenin, cyclin D1, and c-myc proteins. Finally, we demonstrated that IWP-2, an inhibitor of the Wnt/β-catenin signaling pathway, stemmed the pro-inflammatory and anti-autophagy effect of PGRN siRNA in TNF-α-treated HaCaT cells. Collectively, our findings suggest that PGRN is upregulated in psoriasis lesions and that the overexpression of PGRN inhibits the inflammation in keratinocytes induced by TNF-α by negatively regulating the production of inflammatory factors and positively mediating autophagy through the Wnt/β-catenin signaling pathway; this indicated that overexpression of PGRN may be a potential therapeutic option in psoriasis.

Indexed as

AutophagyCell LineGene SilencingHumansInflammationIntercellular Signaling Peptides and ProteinsKeratinocytesProgranulinsPsoriasisRNA, Small InterferingTumor Necrosis Factor-alphaUp-RegulationWnt Signaling PathwayGRN protein, humanIntercellular Signaling Peptides and ProteinsProgranulinsRNA, Small InterferingTumor Necrosis Factor-alphaautophagyinflammatorykeratinocytesprogranulinpsoriasis

Identifiers

PMID27239673
OpenAlexW2415075823

What OpenQuestion holds

Textmetadata
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.