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Janjuha, S. ; Singh, S.P.* ; Tsakmaki, A.* ; Mousavy Gharavy, S.N.* ; Murawala, P.* ; Konantz, J.* ; Birke, S.* ; Hodson, D.J.* ; Rutter, G.A.* ; Bewick, G.A.* ; Ninov, N.

Age-related islet inflammation marks the proliferative decline of pancreatic beta-cells in zebrafish.

eLife 7:e32965 (2018)
Verlagsversion Postprint DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
The pancreatic islet, a cellular community harboring the insulin-producing beta-cells, is known to undergo age-related alterations. However, only a handful of signals associated with aging have been identified. By comparing beta-cells from younger and older zebrafish, here we show that the aging islets exhibit signs of chronic inflammation. These include recruitment of -expressing macrophages and the activation of NF-kB signaling in beta-cells. Using a transgenic reporter, we show that NF-kB activity is undetectable in juvenile beta-cells, whereas cells from older fish exhibit heterogeneous NF-kB activity. We link this heterogeneity to differences in gene expression and proliferation. Beta-cells with high NF-kB signaling proliferate significantly less compared to their neighbors with low activity. The NF-kB signaling cells also exhibit premature upregulation of , an age-related gene that inhibits beta-cell proliferation. Together, our results show that NF-kB activity marks the asynchronous decline in beta-cell proliferation with advancing age.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Cell Biology ; Zebrafish
ISSN (print) / ISBN 2050-084X
e-ISSN 2050-084X
Zeitschrift eLife
Quellenangaben Band: 7, Heft: , Seiten: , Artikelnummer: e32965 Supplement: ,
Verlag eLife Sciences Publications
Begutachtungsstatus
Institut(e) Institute for Pancreatic Beta Cell Research (IPI)