PMID- 30502465
OWN - NLM
STAT- MEDLINE
DCOM- 20190617
LR  - 20190617
IS  - 1095-9947 (Electronic)
IS  - 1050-4648 (Linking)
VI  - 86
DP  - 2019 Mar
TI  - Identification and functional characterization of grass carp (Ctenopharyngodon 
      idella) tumor necrosis factor receptor 2 and its soluble form with potentiality 
      for targeting inflammation.
PG  - 393-402
LID - S1050-4648(18)30780-0 [pii]
LID - 10.1016/j.fsi.2018.11.061 [doi]
AB  - Tumor necrosis factor-alpha (TNF-alpha) signals through two distinct cell surface 
      receptors, TNFR1 and TNFR2 in mammals. In the present study, grass carp Tnfr2 
      (gcTnfr2) was isolated and characterized. Sequence alignment and phylogenetic 
      analysis suggested that gcTnfr2 was a homolog of goldfish and zebrafish Tnfr2. 
      Tissue distribution assay showed gctnfr2 transcripts were expressed in all 
      examined tissues similar to gctnfr1. To functionally characterize the newly 
      cloned molecule, gcTnfr2 was overexpressed in COS7 cell lines and it showed the 
      ability to mediate the recombinant grass carp Tnf (rgcTnf)-alpha-triggered NF-kappaBeta 
      activity and gcil1b promoter activity, clarifying its role in mediating Tnf-alpha 
      signaling. The recombinant soluble form of gcTnfr2 (rgcsTnfr2) was prepared and 
      it was able to interact with rgcTnf-alpha with higher affinity than that of 
      rgcsTnfr1. Moreover, grass carp soluble Tnfr2 (gcsTnfr2) were detected in the 
      culture medium of grass carp head kidney leukocytes (HKLs) and heat-inactivated 
      A. hydrophila challenge significantly induced its production, indicating 
      involvement of gcsTnfr2 in inflammation response. In agreement with this notion, 
      rgcsTnfr2 effectively antagonized the effect of rgcTnf-alpha on il1b mRNA expression 
      in HKLs, suggesting anti-Tnf-alpha property of gcsTnfr2. To strengthen the 
      anti-inflammatory role of soluble Tnfr2, bacteria were injected intraperitoneally 
      in grass carp followed by rgcsTnfr2. Hematoxylin-eosin (HE) staining of head 
      kidney, spleen and intestine showed that rgcsTnfr2 could significantly improve 
      infection-induced histopathological changes. These results functionally 
      identified gcTnfr2 and its soluble form, particularly highlighting the role of 
      gcsTnfr2 against Tnf-alpha-triggered inflammatory signaling. In this line, rgcsTnfr2 
      displayed anti-inflammatory potentiality during infection, thereby providing a 
      powerful mediator of inflammation control in fish.
CI  - Copyright (c) 2018 Elsevier Ltd. All rights reserved.
FAU - Zhang, Shengnan
AU  - Zhang S
AD  - School of Life Science and Technology, Center for Informational Biology, 
      University of Electronic Science and Technology of China, Chengdu, PR China.
FAU - Wang, Xinyan
AU  - Wang X
AD  - School of Life Science and Technology, Center for Informational Biology, 
      University of Electronic Science and Technology of China, Chengdu, PR China.
FAU - Li, Chenglong
AU  - Li C
AD  - School of Life Science and Technology, Center for Informational Biology, 
      University of Electronic Science and Technology of China, Chengdu, PR China.
FAU - Feng, Shiyu
AU  - Feng S
AD  - School of Life Science and Technology, Center for Informational Biology, 
      University of Electronic Science and Technology of China, Chengdu, PR China.
FAU - Zhang, Anying
AU  - Zhang A
AD  - School of Life Science and Technology, Center for Informational Biology, 
      University of Electronic Science and Technology of China, Chengdu, PR China.
FAU - Yang, Kun
AU  - Yang K
AD  - School of Life Science and Technology, Center for Informational Biology, 
      University of Electronic Science and Technology of China, Chengdu, PR China.
FAU - Zhou, Hong
AU  - Zhou H
AD  - School of Life Science and Technology, Center for Informational Biology, 
      University of Electronic Science and Technology of China, Chengdu, PR China. 
      Electronic address: zhouhongzh@uestc.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20181128
PL  - England
TA  - Fish Shellfish Immunol
JT  - Fish & shellfish immunology
JID - 9505220
RN  - 0 (Fish Proteins)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
SB  - IM
MH  - Aeromonas hydrophila/physiology
MH  - Amino Acid Sequence
MH  - Animals
MH  - Fish Diseases/*immunology
MH  - Fish Proteins/chemistry/genetics/immunology
MH  - Gene Expression Profiling/veterinary
MH  - Gene Expression Regulation/*immunology
MH  - Gram-Negative Bacterial Infections/immunology/veterinary
MH  - Immunity, Innate/*genetics
MH  - Inflammation/immunology/veterinary
MH  - Perciformes/*genetics/*immunology
MH  - Phylogeny
MH  - Receptors, Tumor Necrosis Factor, Type II/chemistry/*genetics/*immunology
MH  - Sequence Alignment/veterinary
MH  - Signal Transduction
OTO - NOTNLM
OT  - Anti-inflammation
OT  - Bacterial infection
OT  - Functional identification
OT  - Grass carp
OT  - Soluble form
OT  - Tnf-alpha receptor 2
EDAT- 2018/12/05 06:00
MHDA- 2019/06/18 06:00
CRDT- 2018/12/04 06:00
PHST- 2018/08/12 00:00 [received]
PHST- 2018/10/15 00:00 [revised]
PHST- 2018/11/27 00:00 [accepted]
PHST- 2018/12/05 06:00 [pubmed]
PHST- 2019/06/18 06:00 [medline]
PHST- 2018/12/04 06:00 [entrez]
AID - S1050-4648(18)30780-0 [pii]
AID - 10.1016/j.fsi.2018.11.061 [doi]
PST - ppublish
SO  - Fish Shellfish Immunol. 2019 Mar;86:393-402. doi: 10.1016/j.fsi.2018.11.061. Epub 
      2018 Nov 28.