NLRP3 inflammasome mediates oxidative stress-induced pancreatic islet dysfunction

American Journal of Physiology. Endocrinology and Metabolism
Marina SokolovaHanne Scholz

Abstract

Inflammasomes are multiprotein inflammatory platforms that induce caspase-1 activation and subsequently interleukin (IL)-1β and IL-18 processing. The NLRP3 inflammasome is activated by different forms of oxidative stress, and, based on the central role of IL-1β in the destruction of pancreatic islets, it could be related to the development of diabetes. We therefore investigated responses in wild-type C57Bl/6 (WT) mice, NLRP3-/- mice, and mice deficient in apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC) after exposing islets to short-term hypoxia or alloxan-induced islet damage. NLRP3-deficient islets compared with WT islets had preserved function ex vivo and were protected against hypoxia-induced cell death. Furthermore, NLRP3 and ASC-deficient mice were protected against oxidative stress-induced diabetes caused by repetitive low-dose alloxan administration, and this was associated with reduced β-cell death and reduced macrophage infiltration. This suggests that the beneficial effect of NLRP3 inflammasome deficiency on oxidative stress-mediated β-cell damage could involve reduced macrophage infiltration and activation. To support the role of macrophage activation in alloxan-induced diabetes...Continue Reading

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Citations

Jul 30, 2019·Journal of Cardiovascular Pharmacology·Marina SokolovaPal Aukrust
Jun 17, 2020·Cell Transplantation·Cheng ChenWei Wang
Apr 26, 2020·Scientific Reports·Vanessa LavallardDomenico Bosco
Oct 5, 2019·Journal of Cardiovascular Pharmacology·Marina SokolovaPål Aukrust
Mar 19, 2020·Cells·Justin Hou Ming Yung, Adria Giacca
Feb 7, 2021·International Journal of Molecular Sciences·Natsuki EguchiHirohito Ichii
Apr 4, 2021·Antioxidants·Štěpánka BenákováLydie Plecitá-Hlavatá

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Methods Mentioned

BETA
Assay
ELISA
PCR
FACS
flow cytometry

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Z9
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Zeiss ZEN Lite
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Apoptosis

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