Abstract
Hypoxia (HYP) stimulates angiogenesis (ANG) by promoting expression of many pro‐angiogenic genes, including AR. The role of PPARα in ANG is controversial. A2BR‐induced activation is known to reduce PPARα‐mediated activity but the effect of PPARα activation on A2BR is unknown. Here, we tested that PPARα attenuates adenosine(AD)‐mediated HYP –induced ANG. Using zebrafish embryo, ANG was measured by counting intersegmental vessel (ISV) and dorsal longitudinal anastomotic vessels (DLAV). Under normoxic condition, WY‐14643 (WY, 10 μM), a PPARα agonist, increased ISV (P<0.01) at 28 hpf but NECA (10 μM), a non selective AR agonist showed no effect. Combined exposure of WY 10 or 100 μM or NECA (10μM) decreased ISV at 28 hpf (p<0.01). However, WY (10 μM) +NECA increased DLAV (P<0.001), whereas, WY (100 μM)+NECA decreased DLAV (P<0.05) at 48 hpf. HYP alone increased ANG (72±19%) at 48 hpf. WY(10 μM) showed no effect on ISV but increased DLAV (P<0.05). At 28 hpf WY (10 μM)+NECA decreased ISV (P<0.001). Our data show that activation of PPARα and AR individually promote HYP‐induced ANG, but combined activation inhibits AD‐mediated HYP‐induced ANG.
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