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dc.contributor.author
Nackiewicz, Dominika
dc.contributor.author
Dan, Meixia
dc.contributor.author
Speck, Madeleine
dc.contributor.author
Chow, Samuel Z.
dc.contributor.author
Chen, Yi-Chun
dc.contributor.author
Pospisilik, J. Andrew
dc.contributor.author
Verchere, C. Bruce
dc.contributor.author
Ehses, Jan A.
dc.date.accessioned
2020-01-29T08:20:16Z
dc.date.available
2020-01-24T03:42:53Z
dc.date.available
2020-01-29T08:20:16Z
dc.date.issued
2020-01-24
dc.identifier.other
10.1016/j.isci.2019.100775
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/393611
dc.identifier.doi
10.3929/ethz-b-000393611
dc.description.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.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Elsevier
en_US
dc.rights.uri
http://creativecommons.org/licenses/by-nc-nd/4.0/
dc.title
Islet Macrophages Shift to a Reparative State following Pancreatic Beta-Cell Death and Are a Major Source of Islet Insulin-like Growth Factor-1
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
dc.date.published
2019-12-14
ethz.journal.title
iScience
ethz.journal.volume
23
en_US
ethz.journal.issue
1
en_US
ethz.pages.start
100775
en_US
ethz.size
46 p.
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.identifier.scopus
ethz.publication.place
Amsterdam
en_US
ethz.publication.status
published
en_US
ethz.date.deposited
2020-01-24T03:43:00Z
ethz.source
SCOPUS
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2020-01-29T08:20:30Z
ethz.rosetta.lastUpdated
2020-02-15T23:54:30Z
ethz.rosetta.exportRequired
true
ethz.rosetta.versionExported
true
ethz.COinS
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