| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1928232 | Biochemical and Biophysical Research Communications | 2015 | 5 Pages |
•sPLA2-IIA is correlated with inflammation and LPS up-regulates the expression of sPLA2-IIA.•EX4 could inhibit LPS- or CLP-mediated sPLA2-IIA expression.•EX4 inhibited the expression of sPLA2-IIA by suppression of cPLA2 and ERK 1/2.
Exendin-4 (EX4), a glucagon-like peptide-1 receptor agonist, has been reported to attenuate myocardial ischemia and reperfusion injury and inflammatory or oxidative responses. The expression level of secretory group IIA phospholipase A2 (sPLA2-IIA) is elevated in inflammatory diseases. Lipopolysaccharide (LPS) upregulates the expression of sPLA2-IIA in human umbilical vein endothelial cells (HUVECs). Here, EX4 was examined for its effects on the expression and activity of sPLA2-IIA in HUVECs and mice. Pre-treatment of cells or mice with EX4 inhibited LPS-induced sPLA2-IIA expression and activity. Additionally, EX4 suppressed LPS-induced activation of cytosolic phospholipase A2 (cPLA2) and extracellular signal-regulated kinase (ERK) 1/2. Therefore, these results show that EX4 inhibited LPS-induced expression of sPLA2-IIA by suppressing cPLA2 and ERK 1/2.
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