Platelet-activating factor induces matrix metalloproteinase-9 expression through Ca(2+)- or PI3K-dependent signaling pathway in a human vascular endothelial cell line

• Published in: FEBS letters 2005-11, Vol.579 (28), p.6451-6458
• Main Authors: Ko, Hyun-Mi, Kang, Jee-Hae, Choi, Jung-Hwa, Park, Sung Jun, Bai, Suk, Im, Suhn-Young
• Format: Article
• Language: English
• Subjects: Calcium - metabolism; Cells, Cultured; Endothelial Cells - drug effects; Endothelial Cells - enzymology; Endothelial Cells - metabolism; Endothelium, Vascular - cytology; Endothelium, Vascular - enzymology; Endothelium, Vascular - metabolism; Humans; Matrix Metalloproteinase 9 - metabolism; NF-kappa B - metabolism; Phosphatidylinositol 3-Kinases - antagonists & inhibitors; Phosphatidylinositol 3-Kinases - metabolism; Phosphatidylinositols - metabolism; Platelet Activating Factor - pharmacology; Signal Transduction; Up-Regulation
• ISSN: 0014-5793
• DOI: 10.1016/j.febslet.2005.10.027

Platelet-activating factor (PAF) augments angiogenesis by promoting the synthesis of a variety of angiogenic factors, via the nuclear factor (NF)-kappaB activation. Recently, we reported that PAF upregulates MMP-9 expression in a NF-kappaB-dependent manner. In this study, we investigated the signaling pathway involved in PAF-induced MMP-9 expression in ECV304 cells. Our current data indicate that the Ca(2+)- or phosphatidylinositol 3-kinase (PI3K)-dependent signaling pathway is necessary for PAF-induced MMP-9 expression. Furthermore, PAF-induced NF-kappaB activation was blocked by selective inhibitors of Ca(2+), PI3K, or extracellular signal-regulated kinase (ERK). Our results suggest that PAF-induced MMP-9 expression, in a NF-kappaB-dependent manner, is regulated by Ca(2+), PI3K and ERK signaling pathways.