Evidence map›Paper›PMID 34678204›Full record

ArticleStem cell reports2021

β-Adrenergic signaling induces Notch-mediated salivary gland progenitor cell control.

X Wang, P Serrano Martinez, J H Terpstra, A Shaalan, G B Proctor, F K L Spijkervet, A Vissink, H Bootsma, F G M Kroese, R P Coppes and 1 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Biomedical applications of organoids derived from the digestive system.Frontiers in cell and developmental biology · 2025
    Review
  6. Article
  7. Review
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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

11 authors at 3 institutions in 2 countries.

X WangDepartment of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
P Serrano MartinezDepartment of Biomedical Sciences of Cells and Systems, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands; Department of Radiation Oncology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
J H TerpstraDepartment of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
A ShaalanCentre for Host and Microbiome Interactions, King's College London, London, UK.
G B ProctorCentre for Host and Microbiome Interactions, King's College London, London, UK.
F K L SpijkervetDepartment of Oral and Maxillofacial Surgery, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
A VissinkDepartment of Oral and Maxillofacial Surgery, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
H BootsmaDepartment of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
F G M KroeseDepartment of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
R P CoppesDepartment of Biomedical Sciences of Cells and Systems, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands; Department of Radiation Oncology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
S PringleDepartment of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. Electronic address: s.a.pringle@umcg.nl.
University Medical Center Groningen · NLUniversity of Groningen · NLKing's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

β-Adrenergic signaling blockade is a mainstay of hypertension management. One percent of patients taking β-blockers develop reduced salivary gland (SG) function. Here we investigate the role of SG progenitor cells in β-blocker-induced hyposalivation, using human SG organoid cultures (SGOs). Compared with control SGs, initial low SG progenitor cell yield from patients taking β-blockers was observed. When passaged, these SGOs recovered self-renewal and upregulated Notch pathway expression. Notch signaling was downregulated in situ in β-adrenergic receptor-expressing luminal intercalated duct (ID) cells of patients taking β-blockers. Control SGOs treated with β-adrenergic agonist isoproterenol demonstrated increased proportion of luminal ID SGO cells with active Notch signaling. Control SGOs exposed to isoproterenol differentiated into more mature SGOs (mSGOs) expressing markers of acinar cells. We propose that β-blocker-induced Notch signaling reduction in luminal ID cells hampers their ability to proliferate and differentiate into acinar cells, inducing a persistent hyposalivation in some patients taking β-blocking medication.

Indexed as

Adrenergic beta-AgonistsAdrenergic beta-AntagonistsCell DifferentiationCell ProliferationCells, CulturedHumansIsoproterenolOrganoidsReceptors, AdrenergicReceptors, NotchSalivary GlandsSalivationSignal TransductionStem CellsAdrenergic beta-AgonistsAdrenergic beta-AntagonistsIsoproterenolReceptors, AdrenergicReceptors, Notchhyposalivationprogenitor cellssalivary glandβ-adrenergic signalingβ-blockers

Identifiers

PMID34678204
PMCPMC8581054
OpenAlexW3206184432

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.