Abstract：
BACKGROUND & AIMS:There have been conflicting results on a cell of origin in pancreatic regeneration. These discrepancies predominantly stem from lack of specific markers for the pancreatic precursors/stem cells, as well as differences in the targeted cells and severity of tissue injury in the experimental models so far proposed. We attempted to create a model that used diphtheria toxin receptor (DTR) to ablate specific cell populations, control the extent of injury, and avoid induction of the inflammatory response. METHODS:To target specific types of pancreatic cells, we crossed R26DTR or R26DTR/lacZ mice with transgenic mice that express the Cre recombinase in the pancreas, under control of the Pdx1 (global pancreatic) or elastase (acinar-specific) promoters. RESULTS:Exposure of PdxCre;R26DTR mice to diphtheria toxin resulted in extensive ablation of acinar and endocrine tissues but not ductal cells. Surviving cells within the ductal compartment contributed to regeneration of endocrine and acinar cells via recapitulation of the embryonic pancreatic developmental program. However, following selective ablation of acinar tissue in ElaCreERT2;R26DTR mice, regeneration likely occurred by reprogramming of ductal cells to acinar lineage. CONCLUSIONS:In the pancreas of adult mice, epithelial cells within the ductal compartment contribute to regeneration of endocrine and acinar cells. The severity of injury determines the regenerative mechanisms and cell types that contribute to this process.
journal_name
Gastroenterologyjournal_title
Gastroenterologyauthors
Criscimanna A,Speicher JA,Houshmand G,Shiota C,Prasadan K,Ji B,Logsdon CD,Gittes GK,Esni Fdoi
10.1053/j.gastro.2011.07.003subject
Has Abstractpub_date
2011-10-01 00:00:00pages
1451-62, 1462.e1-6issue
4eissn
0016-5085issn
1528-0012pii
S0016-5085(11)00941-3journal_volume
141pub_type
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