Abstract

Hypoxia, adenosine and cytochrome P‐450 epoxygenase (CYP epoxygenase) are known to upregulate angiogenesis; however, the role of peroxisome proliferator‐activated receptor alpha (PPARα) in angiogenesis is controversial. Epifluorescent microscopy was used to assess angiogenesis by counting the number of intersegmental (ISV) and dorsal longitudinal anastomotic vessels (DLAV) at 28 hours post‐fertilization (hpf). Under normoxic as well as hypoxic conditions, WY‐14643 (10 μM), an agonist of PPARα, stimulated angiogenesis while MK‐886 (0.5 μM), an antagonist of PPARα, blunted these effects. NECA (10 μM), an agonist of adenosine receptor promoted angiogenesis more effectively under hypoxic conditions as ISV increased by 85% (p<0.001) and DLAV by 100 % (p<0.001) under hypoxic condition. MRS‐1706 (10 nM), a selective A2B antagonist, abolished NECA‐induced increase in angiogenesis. NECA‐ or WY‐14643‐induced angiogenesis was also inhibited by PPOH (25 or 50 μM), an inhibitor of epoxygenase. Moreover, MK‐886 (0.5 μM) inhibited NECA‐induced adenosine receptor mediated angiogenesis and MRS‐1706 (10 nM) inhibited WY‐14643‐ induced PPARα‐mediated angiogenesis under hypoxic conditions. We conclude that hypoxia promoted PPARα as well as adenosine receptor‐mediated angiogenesis and activation of PPARα promoted angiogenesis just as activation of A2B receptors through epoxide‐dependent mechanism.

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