期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 117, 期 4, 页码 971-977出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI29988
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资金
- NHLBI NIH HHS [5F31HL071273, F31 HL071273] Funding Source: Medline
- NIDDK NIH HHS [P30 DK050306, DK61215, DK56211, P01 DK049210, P30 DK50306, P01 DK49210, R01 DK056211, DK50306, R01 DK061215, P30 DK019525] Funding Source: Medline
It has been suggested that pancreatic acinar cells can serve as progenitors for pancreatic islets, a concept with substantial implications for therapeutic efforts to increase insulin-producing beta cell mass in patients with diabetes. We report what we believe to be the first in vivo lineage tracing approach to determine the plasticity potential of pancreatic acinar cells. We developed an acinar cell-specific inducible Cre recombinase transgenic mouse, which, when mated with a reporter strain and pulsed with tamoxifen, resulted in permanent and specific labeling of acinar cells and their progeny. During various time periods of observation and using several models to provoke injury, we failed to observe any chase of the labeled cells into the endocrine compartment, indicating that acinar cells do not normally transdifferentiate into islet beta cells in vivo in adult mice. In contrast, we observed a substantial role for replication of preexisting acinar cells in the regeneration of new acinar cells after partial pancreatectomy. These results indicate that mature acinar cells harbor a facultative acinar but not endocrine progenitor capacity.
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