scholarly journals Tetramethylpyrazine Showed Therapeutic Effects on Sepsis-Induced Acute Lung Injury in Rats by Inhibiting Endoplasmic Reticulum Stress Protein Kinase RNA-Like Endoplasmic Reticulum Kinase (PERK) Signaling-Induced Apoptosis of Pulmonary Microvascular Endothelial Cells

2018 ◽  
Vol 24 ◽  
pp. 1225-1231 ◽  
Author(s):  
Wensheng Liu ◽  
Kaizhong Liu ◽  
Shu Zhang ◽  
Lihong Shan ◽  
Jiangfeng Tang
Keyword(s):  
Endothelial Cells ◽  
Endoplasmic Reticulum ◽  
Acute Lung Injury ◽  
Protein Kinase ◽  
Lung Injury ◽  
Endoplasmic Reticulum Stress ◽  
Stress Protein ◽  
Microvascular Endothelial Cells ◽  
Therapeutic Effects ◽  
Induced Apoptosis

Prostaglandin E2 enhances interleukin-8 production via EP4 receptor in human pulmonary microvascular endothelial cells

2012 ◽  
Vol 302 (2) ◽  
pp. L266-L273 ◽  
Author(s):  
Hiromichi Aso ◽  
Satoru Ito ◽  
Akemi Mori ◽  
Masataka Morioka ◽  
Nobukazu Suganuma ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Acute Respiratory Distress Syndrome ◽  
Acute Lung Injury ◽  
Protein Kinase ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Distress Syndrome ◽  
Microvascular Endothelial Cells ◽  
Ep4 Receptor ◽  
Kinase A

Prostaglandin E2 (PGE2) is a bioactive prostanoid implicated in the inflammatory processes of acute lung injury/acute respiratory distress syndrome. This study investigated whether PGE2 can induce production of interleukin (IL)-8, the major chemokine for neutrophil activation, from human pulmonary microvascular endothelial cells (HPMVECs). PGE2 significantly enhanced IL-8 protein production with increases in IL-8 mRNA expression and intracellular cAMP levels. HPMVECs expressed only EP4 receptor mRNA. The PGE2 effects were mimicked by a selective EP4 receptor agonist, ONO-AE1–329, and inhibited by a selective EP4 receptor antagonist, ONO-AE3–208, or a protein kinase A inhibitor, Rp-adenosine 3',5'-cyclic monophosphorothioate triethylamine salt. The specific agonist for EP1, EP2, or EP3 receptor did not induce IL-8 production. PGE2-induced IL-8 production was accompanied by p38 phosphorylation and was significantly inhibited by a p38 inhibitor, SB-203580, but not by an ERK1/2 inhibitor, U-0126, or a JNK inhibitor, SP-600125. Additionally, PGE2 increased cyclooxygenase-2 expression with no change in constitutive cyclooxygenase-1 expression, suggesting possible involvement of an autocrine or paracrine manner. In conclusion, PGE2 enhances IL-8 production via EP4 receptor coupled to Gs protein in HPMVECs. Activation of the cAMP/protein kinase A pathway, followed by p38 activation, is essential for these mechanisms. Because neutrophils play a critical role in the inflammation of acute lung injury/acute respiratory distress syndrome, IL-8 released from the pulmonary microvasculature in response to PGE2 may contribute to pathophysiology of this disease.

scholarly journals Cordyceps Militaris Alleviates Severity of Murine Acute Lung Injury Through miRNAs-Mediated CXCR2 Inhibition

2015 ◽  
Vol 36 (5) ◽  
pp. 2003-2011 ◽  
Author(s):  
Sheng Liu ◽  
Jian Tang ◽  
Lei Huang ◽  
Qirong Xu ◽  
Xiang Ling ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Distress Syndrome ◽  
Mrna Level ◽  
Cordyceps Militaris ◽  
Microvascular Endothelial Cells ◽  
Mouse Lung ◽  
Therapeutic Effects ◽  
Beneficial Effects

Background/Aims: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are lethal diseases in humans, and the current treatments have limited therapeutic effects. Cordyceps militaris (CM) is a caterpillar-grown traditional medicinal mushroom, and has been used as a natural invigorant for longevity, endurance, and vitality in China. Recently, purified extracts from CM have been shown to have beneficial effects on various diseases including cancer. Nevertheless, a role of CM in ALI has not been examined previously. Methods: Here, we used a bleomycin-induced ALI model to study the effects of CM on the severity of ALI in mice. The levels of CXCR2, a receptor for Interleukin 8 (IL-8) in pulmonary microvascular endothelial cells, were examined in different experimental groups. The levels of microRNA (miR)-1321 and miR-3188 were also examined in lung samples and in CM. Adeno-associated viruses carrying miR-1321 and miR-3188 were injected into bleomycin-treated mice for evaluation their effects on the severity of ALI. Results: CM treatment significantly alleviated the severity of bleomycin-induced ALI in mice. The increases in lung CXCR2 by bleomycin were significantly reduced by CM at protein level, but not at mRNA level. CM contained high levels of 2 miRNAs (miR-1321 and miR-3188) that target 3'-UTR of CXCR2 mRNA to inhibit its expression. Overexpression of miR-1321 and miR-3188 in mouse lung through AAV-mediated gene therapy mimicked the effects of CM. Conclusion: CM may alleviate severity of murine ALI through miRNAs-mediated CXCR2 inhibition.

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