Cited by 303Pancreatic function and diabetesPancreatic and Hepatic Oncology ResearchPancreatitis Pathology and Treatment

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Preexisting pancreatic acinar cells contribute to acinar cell, but not islet β cell, regeneration

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Desai, Biva M., Oliver-Krasinski, Jennifer, De Leon, Diva D., Farzad, Cyrus, Hong, Nankang, Leach, Steven D., Stoffers, Doris A.·2007·Journal of Clinical Investigation

DOI 10.1172/jci29988PMC PMC1838936

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Abstract

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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Authors: Desai, B. M., Oliver-Krasinski, J., De Leon, D. D., Farzad, C., Hong, N., Leach, S. D., & Stoffers, D. A.
Affiliations: University of Pennsylvania (US)
Johns Hopkins University (US)
Corresponding author: Stoffers, Doris A.
ORCID: Leach, Steven D.
Stoffers, Doris A.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2007-04-02
Volume: 117
Issue: 4
Pages: 971-977
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci29988
PMC: PMC1838936
OpenAlex: W1967081779
Cited by: 303
References: 32
Citations by year: 2026: 2 · 2025: 9 · 2024: 7 · 2023: 10 · 2022: 6 · 2021: 19 · 2020: 17 · 2019: 12 · 2018: 12 · 2017: 8 · 2016: 21 · 2015: 17 · 2014: 20 · 2013: 23 · 2012: 16
FWCI: 25.96
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: American Diabetes Association
National Institutes of Health (5f31hl071273-02)
National Heart, Lung, and Blood Institute (5F31HL071273, F31 HL071273)
National Institute of Diabetes and Digestive and Kidney Diseases (DK56211, R01DK056211, DK-50306, P01-DK49210, DK61215, P01DK049210, R01DK061215, P30DK50306, P30DK019525, P30DK050306)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
Health Sciences › Medicine › Surgery › Pancreatitis Pathology and Treatment
Keywords: pancreatic acinar cells, beta cell regeneration, islet regeneration, transdifferentiation, lineage tracing, inducible Cre recombinase, partial pancreatectomy, pancreatic progenitor cells, cellular plasticity, diabetes mellitus
MeSH terms: Animals, Digestive System Physiological Phenomena, Mice, Transgenic, Organ Specificity, Pancreas, Regeneration, Tamoxifen, Integrases, Reverse Transcriptase Polymerase Chain Reaction, Insulin-Secreting Cells, Mice, Rats

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Preexisting pancreatic acinar cells contribute to acinar cell, but not islet β cell, regeneration

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