Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0071277
Title: Altered Islet Morphology but Normal Islet Secretory Function In Vitro in a Mouse Model with Microvascular Alterations in the Pancreas
Authors: Kostromina E.
Wang X.
Han W. 
Keywords: glucagon
STAT3 protein
animal tissue
article
cellular distribution
controlled study
female
glucose intolerance
immunohistochemistry
in vitro study
insulin release
microvasculature
mouse
nonhuman
organogenesis
pancreas islet
pancreas islet alpha cell
pancreas secretion
signal transduction
Animals
Female
Glucose
Insulin
Islets of Langerhans
Mice
Mice, Knockout
Microvessels
Pancreas
STAT3 Transcription Factor
Issue Date: 2013
Publisher: Public Library of Science
Citation: Kostromina E., Wang X., Han W. (2013). Altered Islet Morphology but Normal Islet Secretory Function In Vitro in a Mouse Model with Microvascular Alterations in the Pancreas. PLoS ONE 8 (7) : e71277. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0071277
Abstract: Background:Our previous studies have shown that signal transducer and activator of transcription 3 (STAT3) signaling is important for the development of pancreatic microvasculature via its regulation of vascular endothelial growth factor-A (VEGF-A). Pancreas-specific STAT3-KO mice exhibit glucose intolerance and impaired insulin secretion in vivo, along with microvascular alterations in the pancreas. However, the specific role of STAT3 signaling in the regulation of pancreatic islet development and function is not entirely understood.Methodology/Principal Findings:To investigate the role of STAT3 signaling in the formation and maintenance of pancreatic islets, we studied pancreas-specific STAT3-KO mice. Histological analysis showed that STAT3 deficiency affected pancreatic islet morphology. We found an increased proportion of small-sized islets and a reduced fraction of medium-sized islets, indicating abnormal islet development in STAT3-KO mice. Interestingly, the islet area relative to the whole pancreas area in transgenic and control mice was not significantly different. Immunohistochemical analysis on pancreatic cryosections revealed abnormalities in islet architecture in STAT3-KO mice: the pattern of peripheral distribution of glucagon-positive ?-cells was altered. At the same time, islets belonging to different size categories isolated from STAT3-KO mice exhibited normal glucose-stimulated insulin secretion in perifusion experiments in vitro when compared to control mice.Conclusions:Our data demonstrate that STAT3 signaling in the pancreas is required for normal islet formation and/or maintenance. Altered islet size distribution in the KO mice does not result in an impaired islet secretory function in vitro. Therefore, our current study supports that the glucose intolerance and in vivo insulin secretion defect in pancreas-specific STAT3-KO mice is due to altered microvasculature in the pancreas, and not intrinsic beta-cell function. © 2013 Kostromina et al.
Source Title: PLoS ONE
URI: https://scholarbank.nus.edu.sg/handle/10635/166194
ISSN: 19326203
DOI: 10.1371/journal.pone.0071277
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