A 24-h
hypoxia exposure experiment was conducted to determine how
hypoxia exposure induce liver angiogenesis in largemouth bass.
Nitrogen (N2) was pumped into water to exclude dissolved
oxygen into 1.2 ± 0.2 mg/L, and liver tissues were sampled during
hypoxia exposure of 0 h, 4 h, 8 h, 12 h, 24 h and re-oxygenation for 12 h. Firstly, the results showed that
hypoxia exposure promoted the angiogenesis occurrence by immunohistochemical analysis of
vascular endothelial growth factor receptor 2 (VEGFR2). Secondly, the concentration of vasodilation factor increased and it's activity was elevated during 8 h exposure, such as
nitric oxide (NO) and
nitric oxide synthase (NOS) (p < 0.05). Thirdly,
hypoxia exposure promoted angiogenesis through up-regulation the expression of
matrix metalloproteinase 2 (MMP-2), jagged,
protein kinase B (AKT), phosphoinositide-3-kinase (PI3K),
mitogen-activated protein kinase (MAPK) at 4 h; contrarily, the expression of inhibiting angiogenesis genes presented up-regulated at 8 h (p < 0.05), such as
matrix metalloproteinase inhibitor-2 (TIMP-2),
matrix metalloproteinase inhibitor-3 (TIMP-3). Finally, the genes and
proteins that regulate angiogenesis presented obvious chronological order. Parts of them promoted the budding and extension of blood vessels were up-regulated during 4 h-8 h (p < 0.05), such as
vascular endothelial growth factor a (VEGFA), VEGFR2, monocarboxylic
acid transporter 1 (MCT1), CD147,
prolyl hydroxylase (PHD),
nuclear factor kappa-B (NF-κB); other part of them promoted blood vessel maturation were highly expressed during 12 h-24 h (p < 0.05), such as
angiogenin-1 (Ang-1) and angiogenin-2 (Ang-2). In short, acute
hypoxia can promote the liver angiogenesis of largemouth bass by HIF - dependent pathway.