Limits...
Involvement of COX-2/PGE2 signalling in hypoxia-induced angiogenic response in endothelial cells.

Zhao L, Wu Y, Xu Z, Wang H, Zhao Z, Li Y, Yang P, Wei X - J. Cell. Mol. Med. (2012)

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.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Oral Diseases, Department of Orthodontics, West China College of Stomatology, Sichuan University, Chengdu, China.

Show MeSH

Related in: MedlinePlus

Effect of NS398, exogenous PGE2 and combinational treatment of NS398 and exogenous PGE2 on cell viability and VEGF, AQP1 mRNA transcription of HUVECs under normoxia or hypoxia. HUVECs were treated with 10 μM of NS398 and/or 10 μM of exogenous PGE2 under normoxia or hypoxia for 3 hrs. Cells without NS398 or exogenous PGE2 treatment served as control. (A) HUVECs proliferation and viability was measured by MTT assay. (B) VEGF mRNA level assessed by real-time RT-PCR experiment. (C) AQP1 mRNA level assessed by real-time RT-PCR experiment. *P < 0.05 and **P < 0.01 versus control.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3822696&req=5

fig09: Effect of NS398, exogenous PGE2 and combinational treatment of NS398 and exogenous PGE2 on cell viability and VEGF, AQP1 mRNA transcription of HUVECs under normoxia or hypoxia. HUVECs were treated with 10 μM of NS398 and/or 10 μM of exogenous PGE2 under normoxia or hypoxia for 3 hrs. Cells without NS398 or exogenous PGE2 treatment served as control. (A) HUVECs proliferation and viability was measured by MTT assay. (B) VEGF mRNA level assessed by real-time RT-PCR experiment. (C) AQP1 mRNA level assessed by real-time RT-PCR experiment. *P < 0.05 and **P < 0.01 versus control.

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).


Involvement of COX-2/PGE2 signalling in hypoxia-induced angiogenic response in endothelial cells.

Zhao L, Wu Y, Xu Z, Wang H, Zhao Z, Li Y, Yang P, Wei X - J. Cell. Mol. Med. (2012)

Effect of NS398, exogenous PGE2 and combinational treatment of NS398 and exogenous PGE2 on cell viability and VEGF, AQP1 mRNA transcription of HUVECs under normoxia or hypoxia. HUVECs were treated with 10 μM of NS398 and/or 10 μM of exogenous PGE2 under normoxia or hypoxia for 3 hrs. Cells without NS398 or exogenous PGE2 treatment served as control. (A) HUVECs proliferation and viability was measured by MTT assay. (B) VEGF mRNA level assessed by real-time RT-PCR experiment. (C) AQP1 mRNA level assessed by real-time RT-PCR experiment. *P < 0.05 and **P < 0.01 versus control.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3822696&req=5

fig09: Effect of NS398, exogenous PGE2 and combinational treatment of NS398 and exogenous PGE2 on cell viability and VEGF, AQP1 mRNA transcription of HUVECs under normoxia or hypoxia. HUVECs were treated with 10 μM of NS398 and/or 10 μM of exogenous PGE2 under normoxia or hypoxia for 3 hrs. Cells without NS398 or exogenous PGE2 treatment served as control. (A) HUVECs proliferation and viability was measured by MTT assay. (B) VEGF mRNA level assessed by real-time RT-PCR experiment. (C) AQP1 mRNA level assessed by real-time RT-PCR experiment. *P < 0.05 and **P < 0.01 versus control.
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).

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.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Oral Diseases, Department of Orthodontics, West China College of Stomatology, Sichuan University, Chengdu, China.

Show MeSH
Related in: MedlinePlus