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Lipoxin A4 attenuation of endothelial inflammation response mimicking pancreatitis-induced lung injury

Lv, Wanzhi; Lv, Chongqing; Yu, Suhui; Yang, Yunxiu; Kong, Hongru; Xie, Jianming; Sun, Hongwei; Andersson, Roland LU ; Xu, Dan and Chen, Bicheng, et al. (2013) In Experimental Biology and Medicine 238(12). p.1388-1395
Abstract
Lipoxins (LXs) and their analogues are known to display potent anti-inflammatory actions. Previously, we reported that lipoxin A4 (LXA4) possessed powerful anti-inflammatory properties in acute pancreatitis in rats and that it may ameliorate the concomitant acute lung injury by reducing cytokine generation and inhibiting neutrophil activation. Considering that the vascular endothelium plays an important role during adherence, migration and activation of leukocytes, the present study was designed to investigate the effects of LXA4 on the inflammatory response induced by tumor necrosis factor a (TNF-alpha) in human pulmonary microvascular endothelial cells (HPMECs) and explore the potential mechanisms involved in these processes. We found... (More)
Lipoxins (LXs) and their analogues are known to display potent anti-inflammatory actions. Previously, we reported that lipoxin A4 (LXA4) possessed powerful anti-inflammatory properties in acute pancreatitis in rats and that it may ameliorate the concomitant acute lung injury by reducing cytokine generation and inhibiting neutrophil activation. Considering that the vascular endothelium plays an important role during adherence, migration and activation of leukocytes, the present study was designed to investigate the effects of LXA4 on the inflammatory response induced by tumor necrosis factor a (TNF-alpha) in human pulmonary microvascular endothelial cells (HPMECs) and explore the potential mechanisms involved in these processes. We found that LXA4 markedly down-regulated the expression of monocyte chemotactic protein-1 (MCP-1), E-selectin, and interleukin-6 (IL-6) mRNA, as well as intercellular adhesion molecule-1 (ICAM-1) in TNF-alpha-exposed HPMECs. Moreover, LXA4 inhibited the phosphorylation and nuclear translocation of nuclear factor-kappa B/p65 (NF-kappa B/p65) and phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) in HPMECs following TNF-alpha stimulation. Heme oxygenase-1 (HO-1), a cytoprotective enzyme, was up-regulated by LXA4 in both non- and TNF-alpha-stimulated HPMECs. In conclusion, the protective effects of LXA4 to ALI may be executed through inhibition inflammation pathways of NF-kappa B and p38 MAPK and up-regulation of cytoprotective HO-1. (Less)
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keywords
Human pulmonary microvascular endothelial cells, lipoxin A4, tumor, necrosis factor a, inflammation, nuclear factor-kappa B
in
Experimental Biology and Medicine
volume
238
issue
12
pages
1388 - 1395
publisher
The Society
external identifiers
  • wos:000327510800008
  • scopus:84888424535
ISSN
1535-3702
DOI
10.1177/1535370213502611
language
English
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yes
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94ec2375-2d25-428e-8033-b27182a689d4 (old id 4273341)
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2014-02-10 12:25:32
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2019-01-06 04:28:48
@article{94ec2375-2d25-428e-8033-b27182a689d4,
  abstract     = {Lipoxins (LXs) and their analogues are known to display potent anti-inflammatory actions. Previously, we reported that lipoxin A4 (LXA4) possessed powerful anti-inflammatory properties in acute pancreatitis in rats and that it may ameliorate the concomitant acute lung injury by reducing cytokine generation and inhibiting neutrophil activation. Considering that the vascular endothelium plays an important role during adherence, migration and activation of leukocytes, the present study was designed to investigate the effects of LXA4 on the inflammatory response induced by tumor necrosis factor a (TNF-alpha) in human pulmonary microvascular endothelial cells (HPMECs) and explore the potential mechanisms involved in these processes. We found that LXA4 markedly down-regulated the expression of monocyte chemotactic protein-1 (MCP-1), E-selectin, and interleukin-6 (IL-6) mRNA, as well as intercellular adhesion molecule-1 (ICAM-1) in TNF-alpha-exposed HPMECs. Moreover, LXA4 inhibited the phosphorylation and nuclear translocation of nuclear factor-kappa B/p65 (NF-kappa B/p65) and phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) in HPMECs following TNF-alpha stimulation. Heme oxygenase-1 (HO-1), a cytoprotective enzyme, was up-regulated by LXA4 in both non- and TNF-alpha-stimulated HPMECs. In conclusion, the protective effects of LXA4 to ALI may be executed through inhibition inflammation pathways of NF-kappa B and p38 MAPK and up-regulation of cytoprotective HO-1.},
  author       = {Lv, Wanzhi and Lv, Chongqing and Yu, Suhui and Yang, Yunxiu and Kong, Hongru and Xie, Jianming and Sun, Hongwei and Andersson, Roland and Xu, Dan and Chen, Bicheng and Zhou, Mengtao},
  issn         = {1535-3702},
  keyword      = {Human pulmonary microvascular endothelial cells,lipoxin A4,tumor,necrosis factor a,inflammation,nuclear factor-kappa B},
  language     = {eng},
  number       = {12},
  pages        = {1388--1395},
  publisher    = {The Society},
  series       = {Experimental Biology and Medicine},
  title        = {Lipoxin A4 attenuation of endothelial inflammation response mimicking pancreatitis-induced lung injury},
  url          = {http://dx.doi.org/10.1177/1535370213502611},
  volume       = {238},
  year         = {2013},
}