Evidence map›Paper›PMID 32524335›Full record

ArticleInflammation2020

Knockdown of H19 Inhibits the Pathogenesis of Acne Vulgaris by Targeting the miR-196a/TLR2/NF-κB Axis.

Shuyun Yang, Fumin Fang, Xiuqin Yu, Changzhi Yang, Xiaoping Zhang, Lu Wang, Liping Zhu, Kai Shao, Tingting Zhu

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 22% 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, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Molecules (Basel, Switzerland) · 2022
    Article
  15. Review
  16. Article
  17. Observational
  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

9 authors at 2 institutions in 1 country.

Shuyun Yang *Department of Dermatology, The People's Hospital of Baoshan, Baoshan, Yunnan, China.
Fumin Fang *Department of Dermatology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Xiuqin YuDepartment of Dermatology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Changzhi YangDepartment of Dermatology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Xiaoping ZhangDepartment of Dermatology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Lu WangDepartment of Dermatology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Liping ZhuDepartment of Dermatology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Kai ShaoDepartment of Dermatology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Tingting Zhu *Department of Dermatology, The First Affiliated Hospital of Soochow University, Suzhou, China. zhutt29@163.com.ORCID http://orcid.org/0000-0002-7581-5904
Soochow University · CNBaoshan College · CN

Funding

National Natural Science Foundation of China 81760559National Natural Science Foundation of China 81960563
6 · The paper itself

Abstract

Acne vulgaris (AV) is a chronic inflammatory disease of the pilosebaceous unit, and Propionibacterium acnes (P. acnes) has been implicated in acne inflammation. Numerous studies have shown that non-coding RNAs play important roles in regulating the pathophysiological processes of acne. In addition, the first imprinted long non-coding RNA (lncRNA) identified, H19, plays a critical role in inflammatory disease. However, the expression and role of H19 in AV remain unclear. In this study, we investigated the effects of H19 in keratinocytes and explored the regulatory mechanisms underlying these effects. H19 was upregulated in keratinocytes treated with P. acnes in a concentration-dependent manner. The phosphorylated forms of the nuclear factor (NF)-κB-related proteins IκBα (p-IκBα) and p65 (p-P65) were significantly upregulated after P. acnes treatment. Additionally, secretion of the proinflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-8 was upregulated in a concentration-dependent manner. Knockdown of H19 inhibited the expression of p-IκBα and p-P65 as well as the secretion of TNF-α, IL-6, and IL-8 in keratinocytes treated with P. acnes. Moreover, H19 was found to exert its proinflammatory effects by activating NF-κB. H19, which was localized mainly in the cytoplasm of keratinocytes, facilitated Toll-like receptor 2 (TLR2) expression by acting as a miR-196a sponge. H19 thus promoted the activation of NF-κB and the secretion of inflammatory cytokines through the miR-196a/TLR2 axis. These findings provide novel insight into the pathogenesis of AV.

Indexed as

Acne VulgarisGene Knockdown TechniquesHumansKeratinocytesMicroRNAsNF-kappa BRNA, Long NoncodingToll-Like Receptor 2H19 long non-coding RNAMicroRNAsMIRN196 microRNA, humanNF-kappa BRNA, Long NoncodingTLR2 protein, humanToll-Like Receptor 2acne vulgarisH19inflammationmiR-196aNF-κBP. acnesTLR2

Identifiers

PMID32524335
OpenAlexW3033157153

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.