PMID- 29241623
OWN - NLM
STAT- MEDLINE
DCOM- 20181211
LR  - 20220408
IS  - 1523-1755 (Electronic)
IS  - 0085-2538 (Linking)
VI  - 93
IP  - 3
DP  - 2018 Mar
TI  - Knockout of the interleukin-36 receptor protects against renal 
      ischemia-reperfusion injury by reduction of proinflammatory cytokines.
PG  - 599-614
LID - S0085-2538(17)30767-6 [pii]
LID - 10.1016/j.kint.2017.09.017 [doi]
AB  - IL-36, a newly named member of the IL-1 cytokine family, includes 3 isoforms, 
      IL-36alpha, IL-36beta, and IL-36gamma, all of which bind to a heterodimer containing the 
      IL-36 receptor (IL-36R). Little is known about the role of the IL-36 axis in 
      acute kidney injury (AKI) pathogenesis. Therefore, we evaluated IL-36 function in 
      the bilateral renal ischemia-reperfusion injury model of AKI using IL-36R 
      knockout and wild-type mice. IL-36R was found to be expressed in the kidney, 
      mainly in proximal tubules. In IL-36R knockout mice, plasma creatinine, blood 
      urea nitrogen, and IL-6 levels after ischemia-reperfusion injury were 
      significantly lower than those in wild-type mice. Immunohistological analysis 
      revealed mild tubular injury. IL-36alpha/beta/gamma levels were increased after 
      ischemia-reperfusion injury, and IL-36alpha was expressed in lymphocytes and proximal 
      tubular cells, but post-ischemia-reperfusion injury mRNA levels of IL-6 and TNF-alpha 
      were low in IL-36R knockout mice. In primary cultures of renal tubular epithelial 
      cells, IL-36alpha treatment upregulated NF-kappaB activity and Erk phosphorylation. 
      Notably, in patients with AKI, urine IL-36alpha levels were increased, and IL-36alpha 
      staining in renal biopsy samples was enhanced. Thus, IL-36alpha/IL-36R blockage could 
      serve as a potential therapeutic target in AKI.
CI  - Copyright (c) 2017 International Society of Nephrology. Published by Elsevier Inc. 
      All rights reserved.
FAU - Nishikawa, Hirofumi
AU  - Nishikawa H
AD  - Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, 
      Kochi University, Kohasu, Oko-cho, Nankoku, Japan.
FAU - Taniguchi, Yoshinori
AU  - Taniguchi Y
AD  - Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, 
      Kochi University, Kohasu, Oko-cho, Nankoku, Japan.
FAU - Matsumoto, Tatsuki
AU  - Matsumoto T
AD  - Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, 
      Kochi University, Kohasu, Oko-cho, Nankoku, Japan.
FAU - Arima, Naoki
AU  - Arima N
AD  - Center for Innovative and Translational Medicine, Kochi Medical School, Kochi 
      University, Kohasu, Oko-cho, Nankoku, Japan.
FAU - Masaki, Mamoru
AU  - Masaki M
AD  - Center for Innovative and Translational Medicine, Kochi Medical School, Kochi 
      University, Kohasu, Oko-cho, Nankoku, Japan.
FAU - Shimamura, Yoshiko
AU  - Shimamura Y
AD  - Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, 
      Kochi University, Kohasu, Oko-cho, Nankoku, Japan.
FAU - Inoue, Kosuke
AU  - Inoue K
AD  - Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, 
      Kochi University, Kohasu, Oko-cho, Nankoku, Japan.
FAU - Horino, Taro
AU  - Horino T
AD  - Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, 
      Kochi University, Kohasu, Oko-cho, Nankoku, Japan.
FAU - Fujimoto, Shimpei
AU  - Fujimoto S
AD  - Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, 
      Kochi University, Kohasu, Oko-cho, Nankoku, Japan.
FAU - Ohko, Kentaro
AU  - Ohko K
AD  - Department of Dermatology, Kochi Medical School, Kochi University, Kohasu, 
      Oko-cho, Nankoku, Japan.
FAU - Komatsu, Toshihiro
AU  - Komatsu T
AD  - Department of Immunology, Kochi Medical School, Kochi University, Kohasu, 
      Oko-cho, Nankoku, Japan.
FAU - Udaka, Keiko
AU  - Udaka K
AD  - Department of Immunology, Kochi Medical School, Kochi University, Kohasu, 
      Oko-cho, Nankoku, Japan.
FAU - Sano, Shigetoshi
AU  - Sano S
AD  - Department of Dermatology, Kochi Medical School, Kochi University, Kohasu, 
      Oko-cho, Nankoku, Japan.
FAU - Terada, Yoshio
AU  - Terada Y
AD  - Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, 
      Kochi University, Kohasu, Oko-cho, Nankoku, Japan. Electronic address: 
      terada@kochi-u.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171211
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Cytokines)
RN  - 0 (IL36A protein, human)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-1)
RN  - 0 (NF-kappa B)
RN  - 0 (Receptors, Interleukin-1)
RN  - 0 (interleukin-36 receptor, mouse)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Acute Kidney Injury/genetics/metabolism/pathology/*prevention & control
MH  - Animals
MH  - Cells, Cultured
MH  - Cytokines/genetics/*metabolism
MH  - Disease Models, Animal
MH  - Down-Regulation
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Genetic Predisposition to Disease
MH  - Humans
MH  - Inflammation Mediators/*metabolism
MH  - Interleukin-1/metabolism
MH  - Kidney/*metabolism/pathology
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - NF-kappa B/metabolism
MH  - Phenotype
MH  - Phosphorylation
MH  - Receptors, Interleukin-1/*deficiency/genetics
MH  - Reperfusion Injury/genetics/metabolism/pathology/*prevention & control
MH  - Signal Transduction
OTO - NOTNLM
OT  - IL-36
OT  - IL-36 receptor
OT  - acute kidney injury
OT  - cytokine
OT  - ischemia-reperfusion injury
EDAT- 2017/12/16 06:00
MHDA- 2018/12/12 06:00
CRDT- 2017/12/16 06:00
PHST- 2017/05/20 00:00 [received]
PHST- 2017/08/23 00:00 [revised]
PHST- 2017/09/14 00:00 [accepted]
PHST- 2017/12/16 06:00 [pubmed]
PHST- 2018/12/12 06:00 [medline]
PHST- 2017/12/16 06:00 [entrez]
AID - S0085-2538(17)30767-6 [pii]
AID - 10.1016/j.kint.2017.09.017 [doi]
PST - ppublish
SO  - Kidney Int. 2018 Mar;93(3):599-614. doi: 10.1016/j.kint.2017.09.017. Epub 2017 
      Dec 11.