Fig. 7
- ID
- ZDB-FIG-161027-7
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- Huang et al., 2016 - Sox9b is a mediator of retinoic acid signaling restricting endocrine progenitor differentiation
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β-cell regeneration is accelerated in adult sox9b heterozygous fish. Hematoxylin and eosin stained sections of adult pancreata from: A) wildtype (here on sox9b+/+); and, B sox9bfh313 heterozygotes (here on sox9b+/-). Exocrine (exo) and islet (is). (C, D) Detection of CACs using immunofluorescent detection of Nkx6.1 and GFP on pancreas sections from fish transgenic for the Notch-responsive reporter and either sox9b+/+ (C) or sox9b+/- (D). Double positive (Nkx6.1+/GFP+) cells were quantified and show no significant difference between sox9b+/+ and sox9b+/- (E). (F, G) Immunofluorescent detection of glucagon (green) and insulin (magenta) to label α and β cells in sox9b+/+ (F) and sox9b+/- (G) adult pancreata. (H) α to β ratio showed no significance difference between islet composition from sox9b+/+ and sox9b+/- fish. (I-K) After β-cell ablation, sox9b+/- adult fish showed better capability of β-cell regeneration compared to sox9b+/+. (I) Blood glucose at 7 days post β-cell ablation shows significantly lower blood glucose levels in sox9b+/- (N=13) compared to sox9b+/+ (N=14). (J) Representative immunofluorescent images of single β cells, small β-cell clusters and pre-existing islets. (K) Number of single β cells 7 days post β-cell ablation was significantly higher in sox9b+/- (n=8) than that in sox9b+/+ (n=6). Each dot represents the average number of single β cells observed per section from one fish. 18-20 transverse paraffin sections for each fish were examined. In this manner we analyzed the majority of pancreatic tissue for all 4 lobes. *p<0.05, ****p<0.0001. |
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Reprinted from Developmental Biology, 418(1), Huang, W., Beer, R.L., Delaspre, F., Wang, G., Edelman, H.E., Park, H., Azuma, M., Parsons, M.J., Sox9b is a mediator of retinoic acid signaling restricting endocrine progenitor differentiation, 28-39, Copyright (2016) with permission from Elsevier. Full text @ Dev. Biol.