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

Age-related islet inflammation marks the proliferative decline of pancreatic beta-cells in zebrafish.
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Janjuha S, Singh SP, Tsakmaki A, Mousavy-Gharavy N, Murawala P, Konantz J, Birke S, Hodson DJ, Rutter G, Bewick G, Ninov NN,


Janjuha S, Singh SP, Tsakmaki A, Mousavy-Gharavy N, Murawala P, Konantz J, Birke S, Hodson DJ, Rutter G, Bewick G, Ninov NN, (click to view)

Janjuha S, Singh SP, Tsakmaki A, Mousavy-Gharavy N, Murawala P, Konantz J, Birke S, Hodson DJ, Rutter G, Bewick G, Ninov NN,

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eLife 2018 04 067() doi 10.7554/eLife.32965
Abstract

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 signalingcells 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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