PMID- 28955891
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 2405-5808 (Print)
IS  - 2405-5808 (Electronic)
IS  - 2405-5808 (Linking)
VI  - 7
DP  - 2016 Sep
TI  - RP S19 C-terminal peptide trimer acts as a C5a receptor antagonist.
PG  - 70-76
LID - 10.1016/j.bbrep.2016.05.006 [doi]
AB  - We have demonstrated that ribosomal protein S19 (RP S19) polymer, when 
      crosslinked between Lys122 and Gln137 by activated coagulation factor XIII, acts 
      as a C5a receptor (C5aR) antagonist/agonist. Based on experimental data obtained 
      using RP S19 analog peptide and recombinant protein monomer, we suggested that 
      L(131)DR, I(134)AGQVAAAN and K(143)KH moieties in the RP S19 C-terminus act in, 
      respectively, C5aR binding, penetration of the plasma membrane, and interaction 
      with either an apoptosis-inducing molecule in neutrophils (delta lactoferrin) or 
      a calcium channel-activating molecule (annexin A3) to induce the p38 MAPK pathway 
      in macrophages. Recently, we observed RP S19 trimer in serum. To study the 
      effects of this RP S19 trimer on C5aR, we prepared mutant RP S19 C-terminal 
      peptide (RP S19(122-145)) dimer and trimer, and examined their chemotactic 
      activities and signal transduction pathways in human C5aR-overexpressing squamous 
      cell carcinoma HSC-1 (HSC-1(C5aR)) cells using 24 trans-well chamber and western 
      blotting assays, respectively. HSC-1(C5aR) cells were attracted by RP 
      S19(122-145) dimer and vice versa by RP S19(122-145) trimer. The RP S19(122-145) 
      dimer-induced attraction was competitively blocked by pre-treatment with RP 
      S19(122-145) trimer. Moreover, RP S19(122-145) trimer-induced p38 MAPK 
      phosphorylation was stronger than RP S19(122-145) dimer-induced p38 MAPK 
      phosphorylation. RP S19(122-145) trimer appeared to act as a C5aR antagonist. The 
      agonistic and antagonistic effects of RP S19(122-145) dimers and trimers were 
      reflected by monocytic, THP-1-derived macrophage-like cells. Unlike the C5aR 
      agonist C5a, which acts at the inflammation phase of acute inflammation, RP S19 
      trimer might act as a C5aR antagonist at the resolution phase.
FAU - Nishiura, Hiroshi
AU  - Nishiura H
AD  - Department of Pathology, Hyogo College of Medicine, 1-1 Mukogawa-cho, 
      Nishinomiya, Hyogo 663-8501, Japan.
FAU - Kawakami, Toru
AU  - Kawakami T
AD  - Institute for Protein Research, Osaka University, 3-2 Yamadaoka, Suita, Osaka 
      565-0871, Japan.
FAU - Kawabe, Mutsuki
AU  - Kawabe M
AD  - Department of Pathology, Hyogo College of Medicine, 1-1 Mukogawa-cho, 
      Nishinomiya, Hyogo 663-8501, Japan.
FAU - Kato-Kogoe, Nahoko
AU  - Kato-Kogoe N
AD  - Department of Pathology, Hyogo College of Medicine, 1-1 Mukogawa-cho, 
      Nishinomiya, Hyogo 663-8501, Japan.
FAU - Yamada, Naoko
AU  - Yamada N
AD  - Department of Pathology, Hyogo College of Medicine, 1-1 Mukogawa-cho, 
      Nishinomiya, Hyogo 663-8501, Japan.
FAU - Nakasho, Keiji
AU  - Nakasho K
AD  - Department of Pathology, Hyogo College of Medicine, 1-1 Mukogawa-cho, 
      Nishinomiya, Hyogo 663-8501, Japan.
FAU - Yamanegi, Koji
AU  - Yamanegi K
AD  - Department of Pathology, Hyogo College of Medicine, 1-1 Mukogawa-cho, 
      Nishinomiya, Hyogo 663-8501, Japan.
LA  - eng
PT  - Journal Article
DEP - 20160510
PL  - Netherlands
TA  - Biochem Biophys Rep
JT  - Biochemistry and biophysics reports
JID - 101660999
PMC - PMC5613253
OTO - NOTNLM
OT  - ANXA3, annexin A3
OT  - Antagonist
OT  - C5a receptor
OT  - C5aR, C5a receptor
OT  - ERK1/2, extracellular signal-regulated protein kinases 1/2
OT  - HSC-1C5aR, C5aR-overexpressing human squamous cell carcinoma HSC-1
OT  - Neutrophils
OT  - P38 MAPK
OT  - RP S19, S19 ribosomal protein
OT  - RP S19122-145, mutant RP S19122-145 peptide
OT  - Ribosomal protein S19
OT  - Trimer
OT  - p38 MAPK, p38 mitogen-activated protein kinase
OT  - deltaLf, delta lactoferrin
EDAT- 2016/05/10 00:00
MHDA- 2016/05/10 00:01
PMCR- 2016/05/10
CRDT- 2017/09/29 06:00
PHST- 2016/02/28 00:00 [received]
PHST- 2016/04/30 00:00 [revised]
PHST- 2016/05/09 00:00 [accepted]
PHST- 2017/09/29 06:00 [entrez]
PHST- 2016/05/10 00:00 [pubmed]
PHST- 2016/05/10 00:01 [medline]
PHST- 2016/05/10 00:00 [pmc-release]
AID - S2405-5808(16)30061-9 [pii]
AID - 10.1016/j.bbrep.2016.05.006 [doi]
PST - epublish
SO  - Biochem Biophys Rep. 2016 May 10;7:70-76. doi: 10.1016/j.bbrep.2016.05.006. 
      eCollection 2016 Sep.