Evidence map›Paper›PMID 31962237›Full record

ArticleiScience2020

Islet Macrophages Shift to a Reparative State following Pancreatic Beta-Cell Death and Are a Major Source of Islet Insulin-like Growth Factor-1.

Dominika Nackiewicz, Meixia Dan, Madeleine Speck, Samuel Z Chow, Yi-Chun Chen, J Andrew Pospisilik, C Bruce Verchere, Jan A Ehses

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 67 citations in OpenAlex.

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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

8 authors at 2 institutions in 3 countries.

Dominika NackiewiczDepartment of Surgery, Faculty of Medicine, University of British Columbia, BC Children's Hospital Research Institute, 950 W 28 Avenue, Vancouver V5Z 4H4, Canada.
Meixia DanDepartment of Surgery, Faculty of Medicine, University of British Columbia, BC Children's Hospital Research Institute, 950 W 28 Avenue, Vancouver V5Z 4H4, Canada.
Madeleine SpeckDepartment of Surgery, Faculty of Medicine, University of British Columbia, BC Children's Hospital Research Institute, 950 W 28 Avenue, Vancouver V5Z 4H4, Canada.
Samuel Z ChowDepartment of Surgery, Faculty of Medicine, University of British Columbia, BC Children's Hospital Research Institute, 950 W 28 Avenue, Vancouver V5Z 4H4, Canada.
Yi-Chun ChenDepartment of Surgery, Faculty of Medicine, University of British Columbia, BC Children's Hospital Research Institute, 950 W 28 Avenue, Vancouver V5Z 4H4, Canada.
J Andrew PospisilikVan Andel Research Institute, 333 Bostwick Avenue NE, Grand Rapids, MI 49503, USA.
C Bruce VerchereDepartment of Surgery, Faculty of Medicine, University of British Columbia, BC Children's Hospital Research Institute, 950 W 28 Avenue, Vancouver V5Z 4H4, Canada; Department of Pathology and Laboratory Medicine, BC Children's Hospital Research Institute, 950 W 28 Avenue, Vancouver V5Z 4H4, Canada. Electronic address: bverchere@bcchr.ca.
Jan A EhsesDepartment of Surgery, Faculty of Medicine, University of British Columbia, BC Children's Hospital Research Institute, 950 W 28 Avenue, Vancouver V5Z 4H4, Canada; Department of Health Sciences and Technology, Institute of Food, Nutrition, and Health, Swiss Federal Institute of Technology, ETH Zürich, Schwerzenbach CH-8603, Switzerland. Electronic address: jehses@ethz.ch.
University of British Columbia · CAVan Andel Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages play a dynamic role in tissue repair following injury. Here we found that following streptozotocin (STZ)-induced beta-cell death, mouse islet macrophages had increased Igf1 expression, decreased proinflammatory cytokine expression, and transcriptome changes consistent with macrophages undergoing efferocytosis and having an enhanced state of metabolism. Macrophages were the major, if not sole, contributors to islet insulin-like growth factor-1 (IGF-1) production. Adoptive transfer experiments showed that macrophages can maintain insulin secretion in vivo following beta-cell death with no effects on islet cell turnover. IGF-1 neutralization during STZ treatment decreased insulin secretion without affecting islet cell apoptosis or proliferation. Interestingly, high-fat diet (HFD) combined with STZ further skewed islet macrophages to a reparative state. Finally, islet macrophages from db/db mice also expressed decreased proinflammatory cytokines and increased Igf1 mRNA. These data have important implications for islet biology and pathology and show that islet macrophages preserve their reparative state following beta-cell death even during HFD feeding and severe hyperglycemia.

Indexed as

DiabetologyImmunologySpecialized Functions of Cells

Identifiers

PMID31962237
PMCPMC6971395
OpenAlexW2995142178

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.