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Stanniocalcin 2 alters PERK signalling and reduces cellular injury during cerulein induced pancreatitis in mice by Elena N Fazio; Gabriel E DiMattia; Sami A Chadi; Kristin D Kernohan; Christopher L Pin is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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## Background Stanniocalcin 2 (STC2) is a secreted protein activated by (PKR)-like Endoplasmic Reticulum Kinase (PERK) signalling under conditions of ER stress __in vitro__. Over-expression of STC2 in mice leads to a growth-restricted phenotype; however, the physiological function for STC2 has remained elusive. Given the relationship of STC2 to PERK signalling, the objective of this study was to examine the role of STC2 in PERK signalling __in vivo__. ## Results Since PERK signalling has both physiological and pathological roles in the pancreas, STC2 expression was assessed in mouse pancreata before and after induction of injury using a cerulein-induced pancreatitis (CIP) model. Increased __Stc2__ expression was identified within four hours of initiating pancreatic injury and correlated to increased activation of PERK signalling. To determine the effect of STC2 over-expression on PERK, mice systemically expressing human STC2 (__STC2__^__Tg__^) were examined. __STC2__^__Tg__^ pancreatic tissue exhibited normal pancreatic morphology, but altered activation of PERK signalling, including increases in Activating Transcription Factor (ATF) 4 accumulation and autophagy. Upon induction of

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Author

Elena N Fazio; Gabriel E DiMattia; Sami A Chadi; Kristin D Kernohan; Christopher L Pin

Publisher

BioMed Central; Springer (Biomed Central Ltd.); London: BioMed Central, [2000]-2018.; Springer Science and Business Media LLC (ISSN 1471-2121)

Published

2011

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)