Key result
Urotensin-II drives strong angiogenesis comparable to FGF-2, an effect abolished by UT-R antagonist Palosuran.
Why the study?
The expression and angiogenic role of urotensin-II and its receptor UT-R in rat brain endothelial cells were not fully characterized.
p-value: p=<0.01
Urotensin-II acts as a pro-angiogenic cytokine in endothelial cells via an autocrine-paracrine mechanism.
No immediate clinical implications; hypothesis-generating for UII in cerebrovascular angiogenesis and requires in vivo validation.
Urotensin-II (UII), along its receptor UT-R, is widely expressed in the cardiovascular system, where it exerts regulatory actions under both physiological and pathological conditions. Real-time PCR and immunocytochemistry demonstrated the expression of UII and UT-R as mRNA and protein in rat neuromicrovascular endothelial cells (NECs). UII did not affect the proliferation rate of cultured NECs, but exerted a strong angiogenic action in both an in vitro assay on Matrigel and an in vivo assay on chorioallantoic membrane. The angiogenic effect of UII was similar to that of FGF-2, and was abolished by the UT-R antagonist Palosuran. Collectively, our findings allow us to include UII in the group of cytokines (e.g. endothelin-1 and adrenomedullin), which are expressed in endothelial cells and exert a pro-angiogenic effect acting in an autocrine-paracrine manner.
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Spinazzi et al. (2006) studied Angiogenesis. Urotensin-II vs. Vehicle (PBS) was evaluated on Angiogenic response (in vitro meshwork formation and in vivo blood vessel count) (p=<0.01). Urotensin-II exerts a strong pro-angiogenic action in both in vitro and in vivo assays, comparable to that of FGF-2, which is abolished by the UT-R antagonist Palosuran.
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