PMID- 29288710
OWN - NLM
STAT- MEDLINE
DCOM- 20190513
LR  - 20210510
IS  - 1873-3913 (Electronic)
IS  - 0898-6568 (Linking)
VI  - 43
DP  - 2018 Mar
TI  - HBP induces the expression of monocyte chemoattractant protein-1 via the 
      FAK/PI3K/AKT and p38 MAPK/NF-kappaB pathways in vascular endothelial cells.
PG  - 85-94
LID - S0898-6568(17)30328-5 [pii]
LID - 10.1016/j.cellsig.2017.12.008 [doi]
AB  - Inflammation is characterized by early influx of polymorphonuclear neutrophils 
      (PMNs), followed by a second wave of monocyte recruitment. PMNs mediate monocyte 
      recruitment via their release of heparin binding protein (HBP), which activates 
      CCR2 (CC-chemokine receptor 2) on monocytes. However, the pathways for such 
      signal transmission remain unknown. Accumulating evidences have highlighted the 
      importance of leukocyte-endothelial cell interactions in the initiation of 
      inflammation. In this study, an interesting finding is that HBP enhances the 
      secretion of monocyte chemotactic protein 1(MCP-1), ligand of CCR2, from a third 
      party, the endothelial cells (ECs). HBP-induced increase in MCP-1 production was 
      demonstrated at the protein, mRNA and secretion levels. Exposure of ECs to HBP 
      elicited rapid phosphorylation of FAK/PI3K/AKT and p38 MAPK/NF-kappaB signaling. 
      MCP-1 levels were attenuated during the response to HBP stimulation by 
      pretreatment with a FAK inhibitor (or siRNA), a PI3K inhibitor, an AKT inhibitor, 
      a p38 inhibitor (or siRNA) and two NF-kappaB inhibitors. Additionally, pretreatment 
      with inhibitors to FAK, PI3K and AKT led to a decrease in HBP-induced 
      phosphorylation of p38/NF-kappaB axis. These results showed that HBP induced MCP-1 
      expression via a sequential activation of the FAK/PI3K/AKT pathway and p38 
      MAPK/NF-kappaB axis. Interestingly, the patterns of HBP regulation of the expression 
      of the adhesion molecular VCAM-1 were similar to those seen in MCP-1 after 
      pretreatment with inhibitors (or not). These findings may help to determine key 
      pharmacological points of intervention, thus slowing the progress of 
      inflammatory-mediated responses in certain diseases where inflammation is 
      detrimental to the host.
CI  - Copyright (c) 2017. Published by Elsevier Inc.
FAU - Chang, Mengling
AU  - Chang M
AD  - Department of Burn and Plastic Surgery, Shanghai Jiao Tong University, School of 
      Medicine, Rui Jin Hospital, Shanghai, China.
FAU - Guo, Feng
AU  - Guo F
AD  - Department of Burn and Plastic Surgery, Shanghai Jiao Tong University, School of 
      Medicine, Rui Jin Hospital, Shanghai, China.
FAU - Zhou, Zengding
AU  - Zhou Z
AD  - Department of Burn and Plastic Surgery, Shanghai Jiao Tong University, School of 
      Medicine, Rui Jin Hospital, Shanghai, China.
FAU - Huang, Xiaoqin
AU  - Huang X
AD  - Department of Burn and Plastic Surgery, Shanghai Jiao Tong University, School of 
      Medicine, Rui Jin Hospital, Shanghai, China.
FAU - Yi, Lei
AU  - Yi L
AD  - Department of Orthopaedic Surgery, Fudan University, School of Medicine, 
      Zhongshan Hospital, Shanghai, China.
FAU - Dou, Yi
AU  - Dou Y
AD  - Department of Burn and Plastic Surgery, Shanghai Jiao Tong University, School of 
      Medicine, Rui Jin Hospital, Shanghai, China.
FAU - Huan, Jingning
AU  - Huan J
AD  - Department of Burn and Plastic Surgery, Shanghai Jiao Tong University, School of 
      Medicine, Rui Jin Hospital, Shanghai, China. Electronic address: 
      hjn11410@rjh.com.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171227
PL  - England
TA  - Cell Signal
JT  - Cellular signalling
JID - 8904683
RN  - 0 (AZU1 protein, human)
RN  - 0 (Antimicrobial Cationic Peptides)
RN  - 0 (Blood Proteins)
RN  - 0 (Carrier Proteins)
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Antimicrobial Cationic Peptides/*pharmacology
MH  - Blood Proteins/*pharmacology
MH  - Carrier Proteins/*pharmacology
MH  - Chemokine CCL2/*genetics/metabolism
MH  - Focal Adhesion Protein-Tyrosine Kinases/*metabolism
MH  - Human Umbilical Vein Endothelial Cells/drug effects/*metabolism
MH  - Humans
MH  - NF-kappa B/metabolism
MH  - Phosphatidylinositol 3-Kinases/*metabolism
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Signal Transduction
MH  - Vascular Cell Adhesion Molecule-1/metabolism
MH  - p38 Mitogen-Activated Protein Kinases/*metabolism
OTO - NOTNLM
OT  - Heparin binding protein (HBP)
OT  - Inflammation
OT  - Monocyte chemotactic protein 1(MCP-1)
OT  - Vascular endothelial cells
EDAT- 2017/12/31 06:00
MHDA- 2019/05/14 06:00
CRDT- 2017/12/31 06:00
PHST- 2017/11/18 00:00 [received]
PHST- 2017/12/24 00:00 [accepted]
PHST- 2017/12/31 06:00 [pubmed]
PHST- 2019/05/14 06:00 [medline]
PHST- 2017/12/31 06:00 [entrez]
AID - S0898-6568(17)30328-5 [pii]
AID - 10.1016/j.cellsig.2017.12.008 [doi]
PST - ppublish
SO  - Cell Signal. 2018 Mar;43:85-94. doi: 10.1016/j.cellsig.2017.12.008. Epub 2017 Dec 
      27.