SEC23B is required for pancreatic acinar cell function in adult mice.

Molecular biology of the cell 2017 Jul 15

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Mice with germline absence of SEC23B die perinatally, exhibiting massive pancreatic degeneration. We generated mice with tamoxifen-inducible, pancreatic acinar cell-specific Sec23b deletion. Inactivation of Sec23b exclusively in the pancreatic acinar cells of adult mice results in decreased overall pancreatic weights from pancreatic cell loss (decreased pancreatic DNA, RNA, and total protein content), as well as degeneration of exocrine cells, decreased zymogen granules, and alterations in the endoplasmic reticulum (ER), ranging from vesicular ER to markedly expanded cisternae with accumulation of moderate-density content or intracisternal granules. Acinar Sec23b deletion results in induction of ER stress and increased apoptosis in the pancreas, potentially explaining the loss of pancreatic cells and decreased pancreatic weight. These findings demonstrate that SEC23B is required for normal function of pancreatic acinar cells in adult mice. © 2017 Khoriaty et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

Citation

Rami Khoriaty, Nancy Vogel, Mark J Hoenerhoff, M Dolors Sans, Guojing Zhu, Lesley Everett, Bradley Nelson, Haritha Durairaj, Brooke McKnight, Bin Zhang, Stephen A Ernst, David Ginsburg, John A Williams. SEC23B is required for pancreatic acinar cell function in adult mice. Molecular biology of the cell. 2017 Jul 15;28(15):2146-2154