Figure 3
Figure 3. PGE2 induces angiogenesis via cAMP. (A) PGE2 and PGE1-OH treatment increases cAMP accumulation. HMVECs were treated with PGE2 (in nM), PGE1-OH (in nM), or isoproterenol (ISO; 1μM), and cAMP levels were determined with a cAMP enzyme immunoassay. Each point represents the mean ± SEM of triplicate samples, and experiments were repeated 3 times. (B) cAMP mimetic db-cAMP induces the tube formation. HMVECs were treated with db-cAMP for 6 hours followed by quantitation of branching points, as described. (C) cAMP competitive analog Rp-cAMPS inhibits the PGE2-induced tube formation. HMVECs were treated with Rp-cAMPS in the presence or absence of PGE2 (100nM) for 6 hours followed by quantitation of branching points. Each point represents the mean ± SEM of triplicate samples, and experiments were repeated 3 times. #P < .05 and ##P < .01 versus corresponding treatment in the control group. For all panels, *P < .05, **P < .01, compared with appropriate control group.

PGE2 induces angiogenesis via cAMP. (A) PGE2 and PGE1-OH treatment increases cAMP accumulation. HMVECs were treated with PGE2 (in nM), PGE1-OH (in nM), or isoproterenol (ISO; 1μM), and cAMP levels were determined with a cAMP enzyme immunoassay. Each point represents the mean ± SEM of triplicate samples, and experiments were repeated 3 times. (B) cAMP mimetic db-cAMP induces the tube formation. HMVECs were treated with db-cAMP for 6 hours followed by quantitation of branching points, as described. (C) cAMP competitive analog Rp-cAMPS inhibits the PGE2-induced tube formation. HMVECs were treated with Rp-cAMPS in the presence or absence of PGE2 (100nM) for 6 hours followed by quantitation of branching points. Each point represents the mean ± SEM of triplicate samples, and experiments were repeated 3 times. #P < .05 and ##P < .01 versus corresponding treatment in the control group. For all panels, *P < .05, **P < .01, compared with appropriate control group.

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