Evidence map›Paper›PMID 33527027›Full record

ArticleAmerican journal of translational research2021

PARK2 attenuates house dust mite-induced inflammatory reaction, pyroptosis and barrier dysfunction in BEAS-2B cells by ubiquitinating NLRP3.

Xiahui Ge, Feng Cai, Yan Shang, Feng Chi, Hua Xiao, Jing Xu, Youhui Fu, Chong Bai

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

  1. Molecular mechanisms of NLRP3 inflammasome activation.Experimental & molecular medicine · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. IL-1Mediators of inflammation · 2023
    Review
  19. Review
  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

8 authors at 2 institutions in 1 country.

Xiahui GeDepartment of Respiratory Medicine, Seventh People's Hospital of Shanghai University of TCM Datong Road, Shanghai 200137, PR China.
Feng CaiDepartment of Respiratory Medicine, Seventh People's Hospital of Shanghai University of TCM Datong Road, Shanghai 200137, PR China.
Yan ShangDepartment of Respiratory and Critical Care Medicine, Changhai Hospital, Naval Medical University Changhai Road, Shanghai 200433, PR China.
Feng ChiDepartment of Respiratory Medicine, Seventh People's Hospital of Shanghai University of TCM Datong Road, Shanghai 200137, PR China.
Hua XiaoDepartment of Respiratory Medicine, Seventh People's Hospital of Shanghai University of TCM Datong Road, Shanghai 200137, PR China.
Jing XuDepartment of Respiratory Medicine, Seventh People's Hospital of Shanghai University of TCM Datong Road, Shanghai 200137, PR China.
Youhui FuDepartment of Respiratory Medicine, Seventh People's Hospital of Shanghai University of TCM Datong Road, Shanghai 200137, PR China.
Chong BaiDepartment of Respiratory and Critical Care Medicine, Changhai Hospital, Naval Medical University Changhai Road, Shanghai 200433, PR China.
Shanghai University of Traditional Chinese Medicine · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivePARK2, a Parkinson's disease-associated gene, functions as an E3 ubiquitin ligase regulating the degradation of proteins via ubiquitination. Our study was designed to explore its role in allergic asthma and the underlying mechanisms.

methodsAirway epithelial cell line BEAS-2B was treated with house dust mite (HDM) to mimic allergic asthma in vitro. Lentivirus oePARK2 and siPARK2 were constructed to overexpress and knock down PARK2 expression, respectively. RT-qPCR, western blot, co-immunoprecipitation, and ubiquitination assay were performed to investigate the interaction between PARK2 and NLRP3. NLRP3 inflammasome activity, IL-1β and IL-18 secretion, pyroptosis, and epithelial barrier integrity were detected to explore the role of PARK2 in allergic asthma.

resultsPARK2 expression was remarkably down-regulated in HDM-treated BEAS-2B cells. In BEAS-2B cells, NLRP3 protein was reduced by PARK2 overexpression and increased by PARK2 knockdown. Interestingly, PARK2 overexpression and knockdown didn't affect NLRP3 mRNA. Co-immunoprecipitation assay showed that PARK2 interacted with NLRP3. Proteasome inhibitor MG132 abolished PARK2 overexpression-induced down-regulation of NLRP3 protein. Ubiquitination assays showed that PARK2 overexpression enhanced the ubiquitination of NLRP3. Collectively, PARK2 negatively regulates NLRP3 protein via ubiquitination. In HDM-treated BEAS-2B cells, PARK2 overexpression repressed HDM-induced NLRP3 inflammasome activation, IL-1β and IL-18 secretion, pyroptosis, and epithelial barrier dysfunction. In BEAS-2B cells, PARK2 knockdown promoted NLRP3 inflammasome activation, IL-1β and IL-18 secretion, pyroptosis, and barrier impairment, while its effects were abrogated by NLRP3 inhibitor INF39.

conclusionOur study demonstrates that PARK2 attenuates HDM-induced NLRP3 inflammasome activation, the release of inflammatory cytokines, pyroptosis, and barrier impairment in airway epithelial cells by ubiquitinating NLRP3.

Indexed as

airway epithelial barrier dysfunctioninflammationNLRP3PARK2pyroptosis

Identifiers

PMID33527027
PMCPMC7847526
OpenAlexW3128474096

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.