PMID- 25818598
OWN - NLM
STAT- MEDLINE
DCOM- 20150810
LR  - 20150606
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 286
IP  - 2
DP  - 2015 Jul 15
TI  - Tat-CBR1 inhibits inflammatory responses through the suppressions of NF-kappaB and 
      MAPK activation in macrophages and TPA-induced ear edema in mice.
PG  - 124-34
LID - S0041-008X(15)00111-8 [pii]
LID - 10.1016/j.taap.2015.03.020 [doi]
AB  - Human carbonyl reductase 1 (CBR1) plays a crucial role in cell survival and 
      protects against oxidative stress response. However, its anti-inflammatory 
      effects are not yet clearly understood. In this study, we examined whether CBR1 
      protects against inflammatory responses in macrophages and mice using a Tat-CBR1 
      protein which is able to penetrate into cells. The results revealed that purified 
      Tat-CBR1 protein efficiently transduced into Raw 264.7 cells and inhibited 
      lipopolysaccharide (LPS)-induced cyclooxygenase-2 (COX-2), nitric oxide (NO) and 
      prostaglandin E2 (PGE2) expression levels. In addition, Tat-CBR1 protein leads to 
      decreased pro-inflammatory cytokine expression through suppression of nuclear 
      transcription factor-kappaB (NF-kappaB) and mitogen activated protein kinase (MAPK) 
      activation. Furthermore, Tat-CBR1 protein inhibited inflammatory responses in 
      12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation when applied 
      topically. These findings indicate that Tat-CBR1 protein has anti-inflammatory 
      properties in vitro and in vivo through inhibition of NF-kappaB and MAPK activation, 
      suggesting that Tat-CBR1 protein may have potential as a therapeutic agent 
      against inflammatory diseases.
CI  - Copyright (c) 2015 Elsevier Inc. All rights reserved.
FAU - Kim, Young Nam
AU  - Kim YN
AD  - Department of Biomedical Science and Research Institute of Bioscience and 
      Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea.
FAU - Kim, Dae Won
AU  - Kim DW
AD  - Department of Biochemistry and Molecular Biology, Research Institute of Oral 
      Sciences, College of Dentistry, Kangnung-Wonju National University, Kangneung 
      210-702, Republic of Korea.
FAU - Jo, Hyo Sang
AU  - Jo HS
AD  - Department of Biomedical Science and Research Institute of Bioscience and 
      Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea.
FAU - Shin, Min Jea
AU  - Shin MJ
AD  - Department of Biomedical Science and Research Institute of Bioscience and 
      Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea.
FAU - Ahn, Eun Hee
AU  - Ahn EH
AD  - Department of Biomedical Science and Research Institute of Bioscience and 
      Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea.
FAU - Ryu, Eun Ji
AU  - Ryu EJ
AD  - Department of Biomedical Science and Research Institute of Bioscience and 
      Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea.
FAU - Yong, Ji In
AU  - Yong JI
AD  - Department of Biomedical Science and Research Institute of Bioscience and 
      Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea.
FAU - Cha, Hyun Ju
AU  - Cha HJ
AD  - Department of Biomedical Science and Research Institute of Bioscience and 
      Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea.
FAU - Kim, Sang Jin
AU  - Kim SJ
AD  - Department of Biomedical Science and Research Institute of Bioscience and 
      Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea.
FAU - Yeo, Hyeon Ji
AU  - Yeo HJ
AD  - Department of Biomedical Science and Research Institute of Bioscience and 
      Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea.
FAU - Youn, Jong Kyu
AU  - Youn JK
AD  - Department of Biomedical Science and Research Institute of Bioscience and 
      Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea.
FAU - Hwang, Jae Hyeok
AU  - Hwang JH
AD  - Department of Biomedical Science and Research Institute of Bioscience and 
      Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea.
FAU - Jeong, Ji-Heon
AU  - Jeong JH
AD  - Department of Anatomy, College of Medicine, Soonchunhyang University, Cheonan-Si 
      330-090, Republic of Korea.
FAU - Kim, Duk-Soo
AU  - Kim DS
AD  - Department of Anatomy, College of Medicine, Soonchunhyang University, Cheonan-Si 
      330-090, Republic of Korea.
FAU - Cho, Sung-Woo
AU  - Cho SW
AD  - Department of Biochemistry and Molecular Biology, University of Ulsan College of 
      Medicine, Seoul 138-736, Republic of Korea.
FAU - Park, Jinseu
AU  - Park J
AD  - Department of Biomedical Science and Research Institute of Bioscience and 
      Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea.
FAU - Eum, Won Sik
AU  - Eum WS
AD  - Department of Biomedical Science and Research Institute of Bioscience and 
      Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea. Electronic 
      address: wseum@hallym.ac.kr.
FAU - Choi, Soo Young
AU  - Choi SY
AD  - Department of Biomedical Science and Research Institute of Bioscience and 
      Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea. Electronic 
      address: sychoi@hallym.ac.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150325
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Gene Products, tat)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - EC 1.1.- (Alcohol Oxidoreductases)
RN  - EC 1.1.1.184 (CBR1 protein, human)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Alcohol Oxidoreductases/*pharmacology
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Ear, External/pathology
MH  - Edema/chemically induced/*drug therapy/pathology
MH  - Enzyme Activation/drug effects
MH  - Gene Products, tat/*pharmacology
MH  - Lipopolysaccharides
MH  - Macrophages/*drug effects
MH  - Male
MH  - Membrane Potential, Mitochondrial/drug effects
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Mitogen-Activated Protein Kinases/*antagonists & inhibitors
MH  - NF-kappa B/*antagonists & inhibitors
MH  - Subcellular Fractions/drug effects
MH  - Tetradecanoylphorbol Acetate
OTO - NOTNLM
OT  - Apoptosis
OT  - Oxidative stress
OT  - Protein therapy
OT  - Skin inflammation
OT  - Tat-CBR1
EDAT- 2015/03/31 06:00
MHDA- 2015/08/11 06:00
CRDT- 2015/03/31 06:00
PHST- 2014/09/10 00:00 [received]
PHST- 2015/03/05 00:00 [revised]
PHST- 2015/03/17 00:00 [accepted]
PHST- 2015/03/31 06:00 [entrez]
PHST- 2015/03/31 06:00 [pubmed]
PHST- 2015/08/11 06:00 [medline]
AID - S0041-008X(15)00111-8 [pii]
AID - 10.1016/j.taap.2015.03.020 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2015 Jul 15;286(2):124-34. doi: 
      10.1016/j.taap.2015.03.020. Epub 2015 Mar 25.