Archived
This content is available here strictly for research, reference, and/or recordkeeping and as such it may not be fully accessible. If you work or study at University of Kentucky and would like to request an accessible version, please use the SensusAccess Document Converter.
Abstract
Bacterial endotoxin has been known to induce excessive inflammatory responses and acute kidney injury. In the present study, we used a mouse model of endotoxemia to investigate the role of Sirt1 in inflammatory kidney injury. We examined molecular and cellular responses in inducible Sirt1 knockout (Sirt1-/-) mice and wild type littermates (Sirt1+/+) in lipopolysaccharide (LPS)-induced kidney injury. Our studies demonstrated that Sirt1 deletion caused aggravated kidney injury, which was associated with increased inflammatory responses including elevated pro-inflammatory cytokine production, and increased ICAM-1 and VCAM-1 expression. Inflammatory signaling such as STAT3/ERK phosphorylation and NF-κB activation was markedly elevated in kidney tissues of Sirt1 knockout mice after LPS challenge. The results indicate that Sirt1 is protective against LPS-induced acute kidney injury by suppressing kidney inflammation and down-regulating inflammatory signaling.
Document Type
Article
Publication Date
5-4-2014
Digital Object Identifier (DOI)
http://dx.doi.org/10.1371/journal.pone.0098909
Repository Citation
Gao, Rong; Chen, Jiao; Hu, Yuxin; Li, Zhenyu; Wang, Shuxia; Shetty, Sreerama; and Fu, Jian, "Sirt1 Deletion Leads to Enhanced Inflammation and Aggravates Endotoxin-Induced Acute Kidney Injury" (2014). Toxicology and Cancer Biology Faculty Publications. 24.
https://uknowledge.uky.edu/toxicology_facpub/24

Notes/Citation Information
Published in PLOS One, v. 9, issue 6, e98909.
© 2014 Gao et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.