| Literature DB >> 29920277 |
Shira Anzi1, Miri Stolovich-Rain1, Agnes Klochendler1, Ori Fridlich1, Aharon Helman1, Avital Paz-Sonnenfeld2, Nili Avni-Magen2, Elizabeth Kaufman2, Miriam B Ginzberg3, Daniel Snider3, Saikat Ray4, Michael Brecht4, Melissa M Holmes5, Karen Meir6, Aaron Avivi7, Imad Shams7, Asaf Berkowitz8, A M James Shapiro9, Benjamin Glaser10, Shmuel Ben-Sasson1, Ran Kafri3, Yuval Dor11.
Abstract
Developmental processes in different mammals are thought to share fundamental cellular mechanisms. We report a dramatic increase in cell size during postnatal pancreas development in rodents, accounting for much of the increase in organ size after birth. Hypertrophy of pancreatic acinar cells involves both higher ploidy and increased biosynthesis per genome copy; is maximal adjacent to islets, suggesting endocrine to exocrine communication; and is partly driven by weaning-related processes. In contrast to the situation in rodents, pancreas cell size in humans remains stable postnatally, indicating organ growth by pure hyperplasia. Pancreatic acinar cell volume varies 9-fold among 24 mammalian species analyzed, and shows a striking inverse correlation with organismal lifespan. We hypothesize that cellular hypertrophy is a strategy for rapid postnatal tissue growth, entailing life-long detrimental effects.Entities:
Keywords: cell size; exocrine pancreas; hyperplasia; hypertrophy; islets; lifespan; nucleolus; postnatal development; salivary glands; weaning
Mesh:
Year: 2018 PMID: 29920277 DOI: 10.1016/j.devcel.2018.05.024
Source DB: PubMed Journal: Dev Cell ISSN: 1534-5807 Impact factor: 12.270