Evidence map›Paper›PMID 24947582›Full record

ArticleDiabetologia2014

A stress response pathway in mice upregulates somatostatin level and transcription in pancreatic delta cells through Gs and β-arrestin 1.

Hong-Mei Wang, Jun-Hong Dong, Qing Li, Qiaoxia Hu, Shang-Lei Ning, Wenshuai Zheng, Min Cui, Tian-Sheng Chen, Xin Xie, Jin-Peng Sun and 1 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  3. Activation of PTH1R alleviates epididymitis and orchitis through Gq and β-arrestin-1 pathways.Proceedings of the National Academy of Sciences of the United States of America · 2021
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  6. Regulatory Mechanisms of Somatostatin Expression.International journal of molecular sciences · 2020
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  11. GPCRs in Autocrine and Paracrine Regulations.Frontiers in endocrinology · 2019
    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 5 institutions in 1 country.

Hong-Mei WangKey Laboratory Experimental Teratology of the Ministry of Education and Department of Physiology, Shandong University School of Medicine, 44 Wenhua Xi Road, Jinan, Shandong, 250012, China.
Jun-Hong Dong
Qing Li
Qiaoxia Hu
Shang-Lei Ning
Wenshuai Zheng
Min Cui
Tian-Sheng Chen
Xin Xie
Jin-Peng Sun
Xiao Yu
Shandong University · CNQilu Hospital of Shandong University · CNHuazhong Agricultural University · CNShanghai Institute of Materia Medica · CNWeifang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisSomatostatin secretion from islet delta cells plays an important role in regulating islet function and is tightly controlled by environmental changes. Activation of the adrenergic system promoted somatostatin secretion from islet delta cells; however, the role of the adrenergic system in regulating somatostatin content and transcription has not been defined. An imbalance between the somatostatin content and its secretion may cause dysfunctions in the islet delta cells. We have investigated the role of the adrenergic system in the modulation of somatostatin content and transcription in pancreatic delta cells and the detailed underlying mechanisms of this regulation.

methodsThe stress hormone adrenaline (epinephrine), specific adrenergic agonists or specific adrenergic antagonists were applied to islets from either wild-type or specific adrenergic receptor knockout mice and pancreatic delta cell lines to investigate their effects on somatostatin content and transcription. The GloSensor assay, quantitative real-time PCR, western blots and the dual luciferase assay were used to monitor the cAMP level, somatostatin expression, activations of kinases and transcriptional factors. Arrb1 knockout mice, specific Creb or Pax6 mutations and specific kinase inhibitors were used to dissect the signalling pathway.

resultsAdrenaline and isoprenaline increased somatostatin content and transcription through the activation of β1-/β2-adrenergic receptors (β1-/β2ARs). The somatostatin content in β1AR(-/-) /β2AR(-/-) (Adrb1/Adrb2 knockout) mice was 50% lower than in β1AR(+/+)/β2AR (+/+) mice. Two parallel signalling pathways, Gs-cAMP-protein kinase A (PKA)-cAMP response element binding protein (CREB) and β-arrestin 1-extracellular signal-related kinase (ERK)-paired box protein 6 (PAX6), cooperatively regulated isoprenaline-induced somatostatin transcription. CONCLUSIONS/

interpretationA stress pathway increased somatostatin content and transcription through β-adrenergic agonism. β-Arrestin1, ERK and PAX6 are important pancreatic delta cell regulators in addition to cAMP, PKA and CREB. Dysfunction of β-adrenergic agonism may impair pancreatic delta cell function.

Indexed as

AnimalsArrestinsbeta-Arrestin 1beta-ArrestinsCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinEye ProteinsHomeodomain ProteinsMicePaired Box Transcription FactorsPAX6 Transcription FactorReceptors, AdrenergicRepressor ProteinsSomatostatinSomatostatin-Secreting CellsArrb1 protein, mouseArrestinsbeta-Arrestin 1beta-ArrestinsCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinEye ProteinsHomeodomain ProteinsPaired Box Transcription FactorsPax6 protein, mousePAX6 Transcription FactorReceptors, AdrenergicRepressor ProteinsSomatostatin

Identifiers

PMID24947582
OpenAlexW2028804629

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.