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. 2016 Jan 6;65(4):981–995. doi: 10.2337/db15-0529

Figure 5.

Figure 5

Cyclin D2, induced by glucose in mouse islets, is sufficient to drive β-cell proliferation. A–D: Glucose increased cyclin D2 protein abundance in whole islets at both 24 and 72 h of exposure at the protein (n = 3; A–C) and RNA (n = 3; D) level. E–G: Adenoviral overexpression of cyclin D2 (MOI 5) for 72 h in dispersed islets increased cyclin D2 abundance (E) and BrdU incorporation (n = 3; F and G) modestly in low glucose but markedly in high glucose. H–M: Glucose induction of cyclin D2 protein abundance (n = 3; H and I) and BrdU incorporation (n = 3; K and L) but not PCNA abundance (n = 3; H and J) was evident, even when MOI of Ad-cyclin D2 was increased as high as 50. M: Cyclin D2 mRNA was increased by high glucose in the context of adenoviral overexpression (dispersed islets, n = 3). Arrows point to BrdU-positive β-cell nuclei. Dotted lines in B–D mark the low glucose control. Data are mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. cyc, cyclin; gluc, glucose; ns, not significant; tub, tubulin.