Extensive elimination of acinar cells during normal postnatal pancreas growth
Summary: While programmed cell death plays important roles during morphogenetic stages of development, post-differentiation organ growth is considered an efficient process whereby cell proliferation increases cell number. Here we demonstrate that early postnatal growth of the pancreas unexpectedly i...
| Main Authors: | , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2023-12-01
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| Series: | Cell Reports |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2211124723014699 |
| _version_ | 1797506344254701568 |
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| author | Miri Stolovich-Rain Ori Fridlich Shira Azulai Agnes Klochendler Shira Anzi Judith Magenheim Ilan Stein Fatima Mushasha Benjamin Glaser Eli Pikarsky Danny Ben-Zvi Yuval Dor |
| author_facet | Miri Stolovich-Rain Ori Fridlich Shira Azulai Agnes Klochendler Shira Anzi Judith Magenheim Ilan Stein Fatima Mushasha Benjamin Glaser Eli Pikarsky Danny Ben-Zvi Yuval Dor |
| author_sort | Miri Stolovich-Rain |
| collection | DOAJ |
| description | Summary: While programmed cell death plays important roles during morphogenetic stages of development, post-differentiation organ growth is considered an efficient process whereby cell proliferation increases cell number. Here we demonstrate that early postnatal growth of the pancreas unexpectedly involves massive acinar cell elimination. Measurements of cell proliferation and death in the human pancreas in comparison to the actual increase in cell number predict daily elimination of 0.7% of cells, offsetting 88% of cell formation over the first year of life. Using mouse models, we show that death is associated with mitosis, through a failure of dividing cells to generate two viable daughters. In p53-deficient mice, acinar cell death and proliferation are reduced, while organ size is normal, suggesting that p53-dependent developmental apoptosis triggers compensatory proliferation. We propose that excess cell turnover during growth of the pancreas, and presumably other organs, facilitates robustness to perturbations and supports maintenance of tissue architecture. |
| first_indexed | 2024-03-10T04:31:20Z |
| format | Article |
| id | doaj.art-f176094f8cba416d8bb0b78d292bb68b |
| institution | Directory Open Access Journal |
| issn | 2211-1247 |
| language | English |
| last_indexed | 2024-03-10T04:31:20Z |
| publishDate | 2023-12-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Cell Reports |
| spelling | doaj.art-f176094f8cba416d8bb0b78d292bb68b2023-11-23T04:28:16ZengElsevierCell Reports2211-12472023-12-014212113457Extensive elimination of acinar cells during normal postnatal pancreas growthMiri Stolovich-Rain0Ori Fridlich1Shira Azulai2Agnes Klochendler3Shira Anzi4Judith Magenheim5Ilan Stein6Fatima Mushasha7Benjamin Glaser8Eli Pikarsky9Danny Ben-Zvi10Yuval Dor11Department of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada (IMRIC), The Hebrew University-Hadassah Medical School, Jerusalem, IsraelDepartment of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada (IMRIC), The Hebrew University-Hadassah Medical School, Jerusalem, IsraelDepartment of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada (IMRIC), The Hebrew University-Hadassah Medical School, Jerusalem, IsraelDepartment of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada (IMRIC), The Hebrew University-Hadassah Medical School, Jerusalem, IsraelDepartment of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada (IMRIC), The Hebrew University-Hadassah Medical School, Jerusalem, IsraelDepartment of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada (IMRIC), The Hebrew University-Hadassah Medical School, Jerusalem, IsraelThe Concern Foundation Laboratories at The Lautenberg Center for Immunology and Cancer Research, Israel-Canada Medical Research Institute, Faculty of Medicine, The Hebrew University, Jerusalem, Israel; Department of Pathology, Hadassah-Hebrew University Medical Center, Jerusalem, IsraelThe Concern Foundation Laboratories at The Lautenberg Center for Immunology and Cancer Research, Israel-Canada Medical Research Institute, Faculty of Medicine, The Hebrew University, Jerusalem, IsraelEndocrinology and Metabolism Service, Department of Internal Medicine, Hadassah-Hebrew University Medical Center, Jerusalem, IsraelThe Concern Foundation Laboratories at The Lautenberg Center for Immunology and Cancer Research, Israel-Canada Medical Research Institute, Faculty of Medicine, The Hebrew University, Jerusalem, Israel; Department of Pathology, Hadassah-Hebrew University Medical Center, Jerusalem, IsraelDepartment of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada (IMRIC), The Hebrew University-Hadassah Medical School, Jerusalem, IsraelDepartment of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada (IMRIC), The Hebrew University-Hadassah Medical School, Jerusalem, Israel; Corresponding authorSummary: While programmed cell death plays important roles during morphogenetic stages of development, post-differentiation organ growth is considered an efficient process whereby cell proliferation increases cell number. Here we demonstrate that early postnatal growth of the pancreas unexpectedly involves massive acinar cell elimination. Measurements of cell proliferation and death in the human pancreas in comparison to the actual increase in cell number predict daily elimination of 0.7% of cells, offsetting 88% of cell formation over the first year of life. Using mouse models, we show that death is associated with mitosis, through a failure of dividing cells to generate two viable daughters. In p53-deficient mice, acinar cell death and proliferation are reduced, while organ size is normal, suggesting that p53-dependent developmental apoptosis triggers compensatory proliferation. We propose that excess cell turnover during growth of the pancreas, and presumably other organs, facilitates robustness to perturbations and supports maintenance of tissue architecture.http://www.sciencedirect.com/science/article/pii/S2211124723014699CP: Developmental biology |
| spellingShingle | Miri Stolovich-Rain Ori Fridlich Shira Azulai Agnes Klochendler Shira Anzi Judith Magenheim Ilan Stein Fatima Mushasha Benjamin Glaser Eli Pikarsky Danny Ben-Zvi Yuval Dor Extensive elimination of acinar cells during normal postnatal pancreas growth Cell Reports CP: Developmental biology |
| title | Extensive elimination of acinar cells during normal postnatal pancreas growth |
| title_full | Extensive elimination of acinar cells during normal postnatal pancreas growth |
| title_fullStr | Extensive elimination of acinar cells during normal postnatal pancreas growth |
| title_full_unstemmed | Extensive elimination of acinar cells during normal postnatal pancreas growth |
| title_short | Extensive elimination of acinar cells during normal postnatal pancreas growth |
| title_sort | extensive elimination of acinar cells during normal postnatal pancreas growth |
| topic | CP: Developmental biology |
| url | http://www.sciencedirect.com/science/article/pii/S2211124723014699 |
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