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Kluth, O.* ; Stadion, M.* ; Gottmann, P.* ; Aga, H.* ; Jähnert, M.* ; Scherneck, S.* ; Vogel, H.* ; Krus, U.* ; Seelig, A. ; Ling, C.* ; Gerdes, J.M. ; Schürmann, A.*

Decreased expression of cilia genes in pancreatic islets as a risk factor for type 2 diabetes in mice and humans.

Cell Rep. 26, 3027-3036.e3 (2019)
Publ. Version/Full Text Research data DOI PMC
Open Access Gold
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An insufficient adaptive beta-cell compensation is a hallmark of type 2 diabetes (T2D). Primary cilia function as versatile sensory antennae regulating various cellular processes, but their role on compensatory beta-cell replication has not been examined. Here, we identify a significant enrichment of downregulated, cilia-annotated genes in pancreatic islets of diabetes-prone NZO mice as compared with diabetes-resistant B6-ob/ob mice. Among 327 differentially expressed mouse cilia genes, 81 human orthologs are also affected in islets of diabetic donors. Islets of nondiabetic mice and humans show a substantial overlap of upregulated cilia genes that are linked to cell-cycle progression. The shRNA-mediated suppression of KIF3A, essential for ciliogenesis, impairs division of MINE beta cells as well as in dispersed primary mouse and human islet cells, as shown by decreased BrdU incorporation. These findings demonstrate the substantial role of cilia-gene regulation on islet function and T2D risk.
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Publication type Article: Journal article
Document type Scientific Article
Keywords New Zealand Obese Mouse ; Beta-cell Proliferation ; Cilia Genes ; Human Pancreatic Islets ; Islet Transcriptomics ; Pathway Enrichment Analysis ; Primary Cilia ; Type 2 Diabetes; Bardet-biedl Syndrome; Obesity; Mechanisms; Differentiation; Ciliopathies; Disruption
Language english
Publication Year 2019
HGF-reported in Year 2019
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Journal Cell Reports
Quellenangaben Volume: 26, Issue: 11, Pages: 3027-3036.e3 Article Number: , Supplement: ,
Publisher Cell Press
Publishing Place 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
Reviewing status Peer reviewed
Institute(s) Institute of Diabetes and Regeneration Research (IDR)
POF-Topic(s) 90000 - German Center for Diabetes Research
Research field(s) Helmholtz Diabetes Center
PSP Element(s) G-501900-233
DOI 10.1016/j.celrep.2019.02.056
WOS ID WOS:000460914700015
Scopus ID 85062366876
PubMed ID 30865891
Erfassungsdatum 2019-03-25
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