Evidence map›Paper›PMID 34239060›Full record

ArticleNature cell biology2021

Niche stiffening compromises hair follicle stem cell potential during ageing by reducing bivalent promoter accessibility.

Janis Koester, Yekaterina A Miroshnikova, Sushmita Ghatak, Carlos Andrés Chacón-Martínez, Jessica Morgner, Xinping Li, Ilian Atanassov, Janine Altmüller, David E Birk, Manuel Koch and 5 more

Abstract read
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In one paragraph

Article in Nature cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
15.8field-weighted citation impact, top 1% 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

63 citing papers in PubMed, 111 citations in OpenAlex.

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3 more citing papers are in PubMed but not listed here.

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

15 authors at 5 institutions in 4 countries.

Janis KoesterMax Planck Institute for Biology of Ageing, Cologne, Germany.ORCID http://orcid.org/0000-0002-5274-0591
Yekaterina A MiroshnikovaMax Planck Institute for Biology of Ageing, Cologne, Germany.
Sushmita GhatakMax Planck Institute for Biology of Ageing, Cologne, Germany.
Carlos Andrés Chacón-MartínezMax Planck Institute for Biology of Ageing, Cologne, Germany.
Jessica MorgnerMax Planck Institute for Biology of Ageing, Cologne, Germany.ORCID http://orcid.org/0000-0001-6374-8639
Xinping LiMax Planck Institute for Biology of Ageing, Cologne, Germany.ORCID http://orcid.org/0000-0002-7427-0017
Ilian AtanassovMax Planck Institute for Biology of Ageing, Cologne, Germany.ORCID http://orcid.org/0000-0001-8259-2545
Janine AltmüllerCologne Center for Genomics, University of Cologne, Cologne, Germany.
David E BirkDepartment of Molecular Pharmacology & Physiology, University of South Florida, Morsani College of Medicine, Tampa, FL, USA.
Manuel KochInstitute for Dental Research and Oral Musculoskeletal Research, Center for Biochemistry, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0002-2962-7814
Wilhelm BlochMolecular and Cellular Sport Medicine, German Sport University Cologne, Cologne, Germany.
Michaela BartuselCenter for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0003-1008-1951
Carien M NiessenCologne Excellence Cluster for Stress Responses in Ageing-associated diseases (CECAD), University of Cologne, Cologne, Germany.
Alvaro Rada-IglesiasCologne Excellence Cluster for Stress Responses in Ageing-associated diseases (CECAD), University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0001-7137-1341
Sara A WickströmMax Planck Institute for Biology of Ageing, Cologne, Germany. sara.wickstrom@helsinki.fi.ORCID http://orcid.org/0000-0001-6383-6292
University of Cologne · DEMax Planck Institute for Biology of Ageing · DEUniversity of Helsinki · FIGerman Sport University Cologne · DEUniversity of South Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tissue turnover requires activation and lineage commitment of tissue-resident stem cells (SCs). These processes are impacted by ageing, but the mechanisms remain unclear. Here, we addressed the mechanisms of ageing in murine hair follicle SCs (HFSCs) and observed a widespread reduction in chromatin accessibility in aged HFSCs, particularly at key self-renewal and differentiation genes, characterized by bivalent promoters occupied by active and repressive chromatin marks. Consistent with this, aged HFSCs showed reduced ability to activate bivalent genes for efficient self-renewal and differentiation. These defects were niche dependent as the transplantation of aged HFSCs into young recipients or synthetic niches restored SC functions. Mechanistically, the aged HFSC niche displayed widespread alterations in extracellular matrix composition and mechanics, resulting in mechanical stress and concomitant transcriptional repression to silence promoters. As a consequence, increasing basement membrane stiffness recapitulated age-related SC changes. These data identify niche mechanics as a central regulator of chromatin state, which, when altered, leads to age-dependent SC exhaustion.

Indexed as

Cell DifferentiationCell Self RenewalCellular SenescenceChromatin Assembly and DisassemblyPromoter Regions, GeneticStem Cell NicheAnimalsCell LineageCells, CulturedExtracellular MatrixGene SilencingHair FollicleMaleMechanotransduction, CellularMiceMice, Inbred C57BL

Identifiers

PMID34239060
OpenAlexW3183123849

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.