Premium
Roles of Prostaglandin E2 and 12‐Hydroxy‐eicosatetraenoic Acid on Promotion of Angiogenesis of Choroid‐retinal Endothelial Cells by Pigment Epithelial Cells and Leukocytes under Inflammatory Conditions
Author(s) -
Tian Haibin,
Lu Yan,
Sherwood Alexander,
Hong Song
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.592.25
Subject(s) - angiogenesis , matrigel , chemistry , microbiology and biotechnology , inflammation , lipid signaling , hydroxyeicosatetraenoic acid , retinal , prostaglandin e2 , biochemistry , biology , arachidonic acid , immunology , cancer research , endocrinology , enzyme
Purposes To determine the effects of choroid‐retinal endothelial cells (CREC), retinal pigment epithelial cells (RPE) and leukocytes on CREC angiogenesis including migration, vasculature formation, and proliferation. The lipid profiles in these process were also determined. Prostaglandin E2 (PGE 2 ) and 12‐hydroxy‐eicosatetraenoic acid (12‐HETE) are chosen as targets to confirm the effects of lipids on CREC angiogenesis. Methods CREC migration was carried out in 24‐transwell plate, RPE or leukocytes in low chambers stimulated with 2ng/ml IL‐1 β and 2ng/ml TNF‐α. Tube formation was performed on matrigel. Lipid profiles of CREC, RPE ad leukocytes were analyzed using LC‐UV‐MS/MS. Results stimulated with IL‐1 β and TNF‐α, EC, RPE and leukocytes could produce many kinds of lipid mediators including PGE 2 and 12HETE, which promoted CREC migration and vasculature formation. CREC and leukocytes produced much more lipid mediators than RPE. High concentration of COX2 inhibitor NS398 and lipoxygenase inhibitor Baicalein inhibited expressions of PGE 2 and 12‐HETE respectively, and subsequently reduce CREC migration and vasculature formation. Conclusions CREC, RPE and leukocytes could promote angiogenesis by producing PGE 2 and 12HETE under inflammation conditions.