Robust angiogenesis in the corpus luteum is critical for maintenance of pregnancy and thus mammalian female fertility. During angiogenesis, blood vessels sprout from pre-existing vasculature and recruit pericytes to induce maturation and vessel quiescence. Pericytes are associated with capillaries and regulate endothelial cell proliferation, vessel diameter, and vascular permeability. Endothelial induction of Notch signaling in adjacent pericytes helps recruit and maintain pericyte coverage in some but not all tissue types. We have employed a Notch decoy, N1^10–24, which blocks Notch signaling in a ligand-specific manner, and determined that pharmacological inhibition of Notch ligand Jagged blocks luteal angiogenesis after normal ovulation, resulting in reduced luteal vasculature. Conversely, after ovarian hyperstimulation, a condition which occurs during fertility treatments, Jagged inhibition causes vascular dilation and hemorrhage. These results indicate that Jagged inhibition has effects in different ovarian angiogenic conditions, promoting vascular growth in the corpus luteum and vascular stability in hyperstimulated ovaries.

中文翻译：

---

锯齿状特定的Notch激活的抑制作用减少黄体生成血管，并引起激素刺激的卵巢黄体出血。

黄体中强大的血管生成对于维持妊娠并因此维持哺乳动物的女性生育能力至关重要。在血管生成过程中，血管从先前存在的脉管系统中萌发，并募集周细胞以诱导成熟和血管静止。周细胞与毛细血管相关，并调节内皮细胞增殖，血管直径和血管通透性。内皮细胞在邻近周细胞中诱导Notch信号有助于在某些而非全部组织类型中募集并维持周细胞覆盖。我们采用了Notch诱饵，N1 ^10–24，其以配体特异性方式阻断Notch信号传导，并确定Notch配体锯齿状的药理学抑制作用可在正常排卵后阻止黄体血管生成，从而导致黄体脉管系统减少。相反，在卵巢过度刺激后，这种情况发生在生育治疗期间，锯齿状抑制作用会引起血管扩张和出血。这些结果表明，锯齿状抑制在不同的卵巢血管生成条件下具有作用，促进黄体中的血管生长和过度刺激的卵巢中​​的血管稳定性。