PMID- 28988112
OWN - NLM
STAT- MEDLINE
DCOM- 20171108
LR  - 20171130
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 494
IP  - 1-2
DP  - 2017 Dec 9
TI  - Caerulin-induced pro-inflammatory response in macrophages requires TRAF3-p38 
      signaling activation.
PG  - 358-364
LID - S0006-291X(17)31979-4 [pii]
LID - 10.1016/j.bbrc.2017.10.017 [doi]
AB  - Acute pancreatitis is a common threat to human health. Caerulin provokes severe 
      inflammations, causing injuries to surrounding pancreatic cells. TNF 
      receptor-associated factor 3 (TRAF3) is a highly versatile regulator of immune 
      response. The current study aims to understand the potential effect of TRAF3 on 
      caerulin-induced pro-inflammatory responses. In the primary-cultured mouse bone 
      marrow-derived macrophages (BMDMs), caerulin induced TRAF3 protein stabilization, 
      which formed a complex with mitogen-activated protein kinase kinase 3 (MKK3) to 
      mediate downstream p38 activation. Lentiviral shRNA-mediated TRAF3 stable 
      knockdown significantly attenuated caerulin-induced MKK3-p38 activation and 
      production of several key pro-inflammatory cytokines, including interleukin-1beta 
      (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and IL-17. Remarkably, TRAF3 knockdown 
      in caerulin-stimulated BMDMs also alleviated cytotoxicity to Panc02 and primary 
      mouse pancreatic cells. Thus, TRAF3 is required for caerulin-induced p38 
      activation and macrophage-mediated pro-inflammatory responses. TRAF3 expression 
      in macrophages could be a novel therapeutic target protein for the treatment of 
      acute pancreatitis.
CI  - Copyright (c) 2017 Elsevier Inc. All rights reserved.
FAU - Jia, Rongrong
AU  - Jia R
AD  - Department of Gastroenterology, Tongren Hospital, Shanghai Jiao Tong University 
      School of Medicine, Shanghai, China.
FAU - Ma, Jiali
AU  - Ma J
AD  - Department of Gastroenterology, Tongren Hospital, Shanghai Jiao Tong University 
      School of Medicine, Shanghai, China.
FAU - Xiang, Shihao
AU  - Xiang S
AD  - Department of Gastroenterology, Tongren Hospital, Shanghai Jiao Tong University 
      School of Medicine, Shanghai, China.
FAU - Meng, Wenying
AU  - Meng W
AD  - Department of Gastroenterology, Tongren Hospital, Shanghai Jiao Tong University 
      School of Medicine, Shanghai, China.
FAU - Wang, Na
AU  - Wang N
AD  - Department of Gastroenterology, Tongren Hospital, Shanghai Jiao Tong University 
      School of Medicine, Shanghai, China. Electronic address: wangna2017_tr@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171005
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (IL1B protein, mouse)
RN  - 0 (Interleukin-17)
RN  - 0 (Interleukin-1beta)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (TNF Receptor-Associated Factor 3)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 888Y08971B (Ceruletide)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - EC 2.7.12.2 (MAP Kinase Kinase 3)
RN  - EC 2.7.12.2 (Map2k3 protein, mouse)
SB  - IM
MH  - Animals
MH  - Ceruletide/*pharmacology
MH  - Coculture Techniques
MH  - Epithelial Cells/cytology/*drug effects/immunology
MH  - Gene Expression Regulation
MH  - Interleukin-17/genetics/immunology
MH  - Interleukin-1beta/genetics/immunology
MH  - Lentivirus/genetics/immunology
MH  - MAP Kinase Kinase 3/genetics/immunology
MH  - Macrophages/cytology/*drug effects/immunology
MH  - Mice
MH  - Pancreas/cytology/drug effects/immunology
MH  - Primary Cell Culture
MH  - RNA, Small Interfering/genetics/immunology
MH  - Signal Transduction/*drug effects
MH  - TNF Receptor-Associated Factor 3/antagonists & inhibitors/*genetics/immunology
MH  - Tumor Necrosis Factor-alpha/genetics/immunology
MH  - p38 Mitogen-Activated Protein Kinases/*genetics/immunology
OTO - NOTNLM
OT  - Acute pancreatitis
OT  - Caerulin
OT  - Macrophages
OT  - Pro-inflammatory responses
OT  - TRAF3
OT  - p38
EDAT- 2017/10/11 06:00
MHDA- 2017/11/09 06:00
CRDT- 2017/10/09 06:00
PHST- 2017/09/28 00:00 [received]
PHST- 2017/10/04 00:00 [accepted]
PHST- 2017/10/11 06:00 [pubmed]
PHST- 2017/11/09 06:00 [medline]
PHST- 2017/10/09 06:00 [entrez]
AID - S0006-291X(17)31979-4 [pii]
AID - 10.1016/j.bbrc.2017.10.017 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2017 Dec 9;494(1-2):358-364. doi: 
      10.1016/j.bbrc.2017.10.017. Epub 2017 Oct 5.