Analysis Tools
endocrine/exocrine glands
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• mice show more TUNEL+ cells in the pancreas at 1 year of age, indicating an increase in apoptosis
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• focal pancreatic damage
• pancreas shows fatty changes
• some mice show focal inflammatory infiltration as well as acinar cell atrophy and develop a more severe phenotype with increasing age
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• earliest anomaly is mild vacuolization of pancreatic acinar cells
• some pancreatic acinar cells cannot maintain morphological structure and rupture; these cells show that Hmgb-1 is translocated from nucleus to cytoplasm indicating cellular injury
• acinar cells show slightly dilated endoplasmic reticula and vacuolization at 5 months of age
• aged mice develop eosinophilic inclusion bodies and increased vacuolization in acinar cells, with some aged mice showing severe vacuolization of acinar cells which are LC3+ autophagic vesicles and most of these large vesicles are autolysosomes
• aged mice show protein aggregates in the cytoplasm of acinar cells, large autophagy vesicles containing undegraded contents, and pronounced ER dilation in some acinar cells
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• slight atrophy of pancreas
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• in some mice
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• chronic fibrotic changes in the pancreas
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• infiltration of CD45+ leukocytes and F4/80+ macrophages in the pancreas
• up to 12 months of age, about 15% of mice show changes characteristic of pancreatitis, however the full spectrum of features of progressive fibrotic pancreatitis is not seen
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• mice show increased severity of caerulein-induced pancreatitis, showing more extensive edema and inflammatory infiltration, and necrosis
• mice develop more severe chronic pancreatitis after long-term intermittent administration of caerulein, showing acinar cell atrophy, pancreatic duct dilation, immune cell infiltration, and extensive collagen deposition
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cellular
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• increase in autophagy in pancreatic acinar cells at 24 weeks of age but not at 8 weeks of age
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• mice show more TUNEL+ cells in the pancreas at 1 year of age, indicating an increase in apoptosis
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• pancreatic tissue shows increased expression of ER stress markers
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digestive/alimentary system
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• earliest anomaly is mild vacuolization of pancreatic acinar cells
• some pancreatic acinar cells cannot maintain morphological structure and rupture; these cells show that Hmgb-1 is translocated from nucleus to cytoplasm indicating cellular injury
• acinar cells show slightly dilated endoplasmic reticula and vacuolization at 5 months of age
• aged mice develop eosinophilic inclusion bodies and increased vacuolization in acinar cells, with some aged mice showing severe vacuolization of acinar cells which are LC3+ autophagic vesicles and most of these large vesicles are autolysosomes
• aged mice show protein aggregates in the cytoplasm of acinar cells, large autophagy vesicles containing undegraded contents, and pronounced ER dilation in some acinar cells
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• in some mice
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homeostasis/metabolism
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• increase in autophagy in pancreatic acinar cells at 24 weeks of age but not at 8 weeks of age
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immune system
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• infiltration of CD45+ leukocytes and F4/80+ macrophages in the pancreas
• up to 12 months of age, about 15% of mice show changes characteristic of pancreatitis, however the full spectrum of features of progressive fibrotic pancreatitis is not seen
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• mice show increased severity of caerulein-induced pancreatitis, showing more extensive edema and inflammatory infiltration, and necrosis
• mice develop more severe chronic pancreatitis after long-term intermittent administration of caerulein, showing acinar cell atrophy, pancreatic duct dilation, immune cell infiltration, and extensive collagen deposition
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| pancreatitis | DOID:4989 |
OMIM:167800 |
J:338873 | |
