Evidence map›Paper›PMID 31898934›Full record

ArticleeLife2020

Hair follicle stem cells regulate retinoid metabolism to maintain the self-renewal niche for melanocyte stem cells.

Zhiwei Lu, Yuhua Xie, Huanwei Huang, Kaiju Jiang, Bin Zhou, Fengchao Wang, Ting Chen

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Retinoic acid drives hair follicle stem cell activation via Wnt/β-catenin signalling in androgenetic alopecia.Journal of the European Academy of Dermatology and Venereology : JEADV · 2025
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Biology of melanocytes in mammals.Frontiers in cell and developmental biology · 2023
    Review
  14. Review
  15. The landscape of aging.Science China. Life sciences · 2022
    Review
  16. Review
  17. Article
  18. Review
  19. 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

7 authors at 3 institutions in 1 country.

Zhiwei LuPeking Union Medical College, Beijing, China.ORCID 0000-0003-1777-4611
Yuhua XieNational Institute of Biological Sciences, Beijing, China.ORCID 0000-0002-2014-7320
Huanwei HuangNational Institute of Biological Sciences, Beijing, China.
Kaiju JiangNational Institute of Biological Sciences, Beijing, China.
Bin ZhouInstitute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Beijing, China.
Fengchao WangNational Institute of Biological Sciences, Beijing, China.
Ting ChenNational Institute of Biological Sciences, Beijing, China.ORCID 0000-0002-7404-4538
National Institute of Biological Sciences, Beijing · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNShanghai Institutes for Biological Sciences · CN

Funding

National Basic Research Program of China (973 Program) 2012CB518700National Basic Research Program of China (973 Program) 2014CB849602National Key R&D Program of China 2017YFA0103500
6 · The paper itself

Abstract

Metabolites are major biological parameters sensed by many cell types in vivo, whether they function as signaling mediators of SC and niche cross talk to regulate tissue regeneration is largely unknown. We show here that deletion of the Notch pathway co-factor RBP-J specifically in mouse HFSCs triggers adjacent McSCs to precociously differentiate in their shared niche. Transcriptome screen and in vivo functional studies revealed that the elevated level of retinoic acid (RA) caused by de-repression of RA metabolic process genes as a result of RBP-J deletion in HFSCs triggers ectopic McSCs differentiation in the niche. Mechanistically the increased level of RA sensitizes McSCs to differentiation signal KIT-ligand by increasing its c-Kit receptor protein level in vivo. Using genetic approach, we further pinpointed HFSCs as the source of KIT-ligand in the niche. We discover that HFSCs regulate the metabolite RA level in vivo to allow self-renewal of neighboring McSCs.

Indexed as

Stem Cell NicheAnimalsCell DifferentiationHair FollicleMelanocytesMiceMice, TransgenicRetinoidsStem CellsRetinoidsanti-differentiationcell biologydevelopmental biologymetabolitemousestem cell

Identifiers

PMID31898934
PMCPMC6970533
OpenAlexW2997228001

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.