Evidence map›Paper›PMID 31152465›Full record

ArticleCell proliferation2019

Jarid1b promotes epidermal differentiation by mediating the repression of Ship1 and activation of the AKT/Ovol1 pathway.

Xuewei Sun, Zhiyuan Li, Yanfang Niu, Lijuan Zhao, Yichuan Huang, Qiang Li, Shengnan Zhang, Ting Chen, Tao Fu, Tao Yang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Loss of Inpp5d has disease-relevant and sex-specific effects on glial transcriptomes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  3. Article
  4. Review
  5. Epigenetic Mechanisms of Epidermal Differentiation.International journal of molecular sciences · 2022
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. 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

13 authors at 3 institutions in 1 country.

Xuewei SunDepartment of Otolaryngology-Head and Neck Surgery, Key Laboratory, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Zhiyuan LiDepartment of Otolaryngology-Head and Neck Surgery, Key Laboratory, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Yanfang NiuDepartment of Otolaryngology-Head and Neck Surgery, Key Laboratory, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Lijuan ZhaoDepartment of Otolaryngology-Head and Neck Surgery, Key Laboratory, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Yichuan HuangDepartment of Otolaryngology-Head and Neck Surgery, Key Laboratory, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Qiang LiDepartment of Andrology, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Shengnan ZhangDepartment of Otolaryngology-Head and Neck Surgery, Key Laboratory, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Ting ChenDepartment of Otolaryngology-Head and Neck Surgery, Key Laboratory, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Tao FuDepartment of Otolaryngology-Head and Neck Surgery, Key Laboratory, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Tao YangDepartment of Biochemistry & Molecular Biology, Shanxi Medical University, Taiyuan, China.
Xiaofei AnDepartment of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.
Yan JiangDepartment of Otolaryngology-Head and Neck Surgery, Key Laboratory, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Jisheng ZhangDepartment of Otolaryngology-Head and Neck Surgery, Key Laboratory, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.ORCID https://orcid.org/0000-0001-9674-8483
Qingdao University · CNNanjing University of Chinese Medicine · CNShanxi Medical University · CN

Funding

National Natural Science Foundation of China 81672662National Natural Science Foundation of China 81701381National Natural Science Foundation of China 81770978National Natural Science Foundation of China 81774248Shandong Provincial Education Department Program J14LK02the Key Research and Development Program of Shandong Province 2017GSF18193the Key Research and Development Program of Shandong Province 2018GSF118012the Natural Science Foundation of Shandong Province ZR2014CM040the Shandong Medical and Health Science and Technology Development Plan 2016WS0268
6 · The paper itself

Abstract

objectivesTerminally differentiated stratified squamous epithelial cells play an important role in barrier protection of the skin. The integrity of epidermal cells is maintained by tight regulation of proliferation and differentiation. The aim of this study was to investigate the role of epigenetic regulator H3K4me3 and its demethylase Jarid1b in the control of epithelial cell differentiation. MATERIALS AND

methodsRT-qPCR, Western blotting and IHC were used to detect mRNA and protein levels. We analysed cell proliferation by CCK8 assay and cell migration by wound healing assay. ChIP was used to measure H3K4me3 enrichment. A chamber graft model was established for epidermal development.

resultsOur studies showed that H3K4me3 was decreased during epidermal differentiation. The H3K4me3 demethylase Jarid1b positively controlled epidermal cell differentiation in vitro and in vivo. Mechanistically, we found that Jarid1b substantially increased the expression of mesenchymal-epithelial transition (MET)-related genes, among which Ovol1 positively regulated differentiation gene expression. In addition, Ovol1 expression was repressed by PI3K-AKT pathway inhibitors and overexpression (O/E) of the PI3K-AKT pathway suppressor Ship1. Knockdown (KD) of Ship1 activated downstream PI3K-AKT pathway and enhanced Ovol1 expression in HaCaT. Importantly, we found that Jarid1b negatively regulated Ship1 expression, but not that of Pten, by directly binding to its promoter to modulate H3K4me3 enrichment.

conclusionOur results identify an essential role of Jarid1b in the regulation of the Ship1/AKT/Ovol1 pathway to promote epithelial cell differentiation.

Indexed as

AnimalsCell DifferentiationCell LineCell ProliferationDNA-Binding ProteinsEpidermal CellsEpithelial-Mesenchymal TransitionHistonesHumansJumonji Domain-Containing Histone DemethylasesMaleMiceMice, NudeNuclear ProteinsPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphatidylinositol 3-KinasesDNA-Binding Proteinshistone H3 trimethyl Lys4HistonesINPP5D protein, humanJumonji Domain-Containing Histone DemethylasesKDM5B protein, humanNuclear ProteinsOVOL1 protein, humanPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRepressor ProteinsRNA, Small InterferingTranscription FactorsdifferentiationepidermisJarid1bOvol1Ship1

Identifiers

PMID31152465
PMCPMC6797505
OpenAlexW2947737902

What OpenQuestion holds

Textmetadata
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.