Involvement of COX-2/PGE2 signalling in hypoxia-induced angiogenic response in endothelial cells.
Bottom Line: The results demonstrated that short-term hypoxic treatment enhanced HUVECs proliferation, migration, tube formation, significantly up-regulated COX-2, VEGF, AQP1 mRNA level, protein expression and promoted PGE(2) , VEGF release.Exogenous PGE(2) augments the effects of hypoxia on HUVECs, and partially reversed the inhibitory effects of NS398 on HUVECs proliferation and angiogenic capability.Short-term hypoxic treatment enhanced angiogenic capability of ECs, and COX-2/PGE(2) signalling may play a critical role in the biological response of ECs to hypoxia.
Affiliation: State Key Laboratory of Oral Diseases, Department of Orthodontics, West China College of Stomatology, Sichuan University, Chengdu, China.Show MeSH
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Mentions: For cell viability, the MTT value of HUVECs under hypoxia was significantly higher than that under normoxia. NS398 exerted a significantly inhibitory effect on HUVECs proliferation both under hypoxia and normoxia, while exogenous PGE2 stimulated them, and combinational treatment of NS398 and PGE2 resulted in a value between the NS398 and PGE2, with hypoxic group significantly higher than the normoxic group (P < 0.05) (Fig. 9A). Similarly, for VEGF and AQP1 mRNA transcription, NS398 alone also significantly blocked while exogenous PGE2 significantly augmented them, and exogenous PGE2 (10 μM) partially reversed the inhibitory effect of NS398 (Fig. 9B and C).
Affiliation: State Key Laboratory of Oral Diseases, Department of Orthodontics, West China College of Stomatology, Sichuan University, Chengdu, China.