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HBP induces the expression of monocyte chemoattractant protein-1 via the FAK/PI3K/AKT and p38 MAPK/NF-κB pathways in vascular endothelial cells.
Cell Signal. 2018 03; 43:85-94.CS

Abstract

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-κB 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-κB inhibitors. Additionally, pretreatment with inhibitors to FAK, PI3K and AKT led to a decrease in HBP-induced phosphorylation of p38/NF-κB axis. These results showed that HBP induced MCP-1 expression via a sequential activation of the FAK/PI3K/AKT pathway and p38 MAPK/NF-κB 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.

Authors+Show Affiliations

Department of Burn and Plastic Surgery, Shanghai Jiao Tong University, School of Medicine, Rui Jin Hospital, Shanghai, China.Department of Burn and Plastic Surgery, Shanghai Jiao Tong University, School of Medicine, Rui Jin Hospital, Shanghai, China.Department of Burn and Plastic Surgery, Shanghai Jiao Tong University, School of Medicine, Rui Jin Hospital, Shanghai, China.Department of Burn and Plastic Surgery, Shanghai Jiao Tong University, School of Medicine, Rui Jin Hospital, Shanghai, China.Department of Orthopaedic Surgery, Fudan University, School of Medicine, Zhongshan Hospital, Shanghai, China.Department of Burn and Plastic Surgery, Shanghai Jiao Tong University, School of Medicine, Rui Jin Hospital, Shanghai, China.Department of Burn and Plastic Surgery, Shanghai Jiao Tong University, School of Medicine, Rui Jin Hospital, Shanghai, China. Electronic address: hjn11410@rjh.com.cn.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

29288710

Citation

Chang, Mengling, et al. "HBP Induces the Expression of Monocyte Chemoattractant Protein-1 Via the FAK/PI3K/AKT and P38 MAPK/NF-κB Pathways in Vascular Endothelial Cells." Cellular Signalling, vol. 43, 2018, pp. 85-94.
Chang M, Guo F, Zhou Z, et al. HBP induces the expression of monocyte chemoattractant protein-1 via the FAK/PI3K/AKT and p38 MAPK/NF-κB pathways in vascular endothelial cells. Cell Signal. 2018;43:85-94.
Chang, M., Guo, F., Zhou, Z., Huang, X., Yi, L., Dou, Y., & Huan, J. (2018). HBP induces the expression of monocyte chemoattractant protein-1 via the FAK/PI3K/AKT and p38 MAPK/NF-κB pathways in vascular endothelial cells. Cellular Signalling, 43, 85-94. https://doi.org/10.1016/j.cellsig.2017.12.008
Chang M, et al. HBP Induces the Expression of Monocyte Chemoattractant Protein-1 Via the FAK/PI3K/AKT and P38 MAPK/NF-κB Pathways in Vascular Endothelial Cells. Cell Signal. 2018;43:85-94. PubMed PMID: 29288710.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - HBP induces the expression of monocyte chemoattractant protein-1 via the FAK/PI3K/AKT and p38 MAPK/NF-κB pathways in vascular endothelial cells. AU - Chang,Mengling, AU - Guo,Feng, AU - Zhou,Zengding, AU - Huang,Xiaoqin, AU - Yi,Lei, AU - Dou,Yi, AU - Huan,Jingning, Y1 - 2017/12/27/ PY - 2017/11/18/received PY - 2017/12/24/accepted PY - 2017/12/31/pubmed PY - 2019/5/14/medline PY - 2017/12/31/entrez KW - Heparin binding protein (HBP) KW - Inflammation KW - Monocyte chemotactic protein 1(MCP-1) KW - Vascular endothelial cells SP - 85 EP - 94 JF - Cellular signalling JO - Cell. Signal. VL - 43 N2 - 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-κB 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-κB inhibitors. Additionally, pretreatment with inhibitors to FAK, PI3K and AKT led to a decrease in HBP-induced phosphorylation of p38/NF-κB axis. These results showed that HBP induced MCP-1 expression via a sequential activation of the FAK/PI3K/AKT pathway and p38 MAPK/NF-κB 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. SN - 1873-3913 UR - https://www.unboundmedicine.com/medline/citation/29288710/HBP_induces_the_expression_of_monocyte_chemoattractant_protein_1_via_the_FAK/PI3K/AKT_and_p38_MAPK/NF_κB_pathways_in_vascular_endothelial_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0898-6568(17)30328-5 DB - PRIME DP - Unbound Medicine ER -