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卵巢中的血管生成和血管功能。

Angiogenesis and vascular function in the ovary.

机构信息

School of Veterinary Medicine and Science Division of Animal Sciences, University of Nottingham, Sutton Bonington Campus, Loughborough, Leicestershire, LE12 5RD, UK.

出版信息

Reproduction. 2009 Dec;138(6):869-81. doi: 10.1530/REP-09-0283. Epub 2009 Sep 28.

Abstract

Ovarian function is dependent on the establishment and continual remodelling of a complex vascular system. This enables the follicle and/or corpus luteum (CL) to receive the required supply of nutrients, oxygen and hormonal support as well as facilitating the release of steroids. Moreover, the inhibition of angiogenesis results in the attenuation of follicular growth, disruption of ovulation and drastic effects on the development and function of the CL. It appears that the production and action of vascular endothelial growth factor A (VEGFA) is necessary at all these stages of development. However, the expression of fibroblast growth factor 2 (FGF2) in the cow is more dynamic than that of VEGFA with a dramatic upregulation during the follicular-luteal transition. This upregulation is then likely to initiate intense angiogenesis in the presence of high VEGFA levels. Recently, we have developed a novel ovarian physiological angiogenesis culture system in which highly organised and intricate endothelial cell networks are formed. This system will enable us to elucidate the complex inter-play between FGF2 and VEGFA as well as other angiogenic factors in the regulation of luteal angiogenesis. Furthermore, recent evidence indicates that pericytes might play an active role in driving angiogenesis and highlights the importance of pericyte-endothelial interactions in this process. Finally, the targeted promotion of angiogenesis may lead to the development of novel strategies to alleviate luteal inadequacy and infertility.

摘要

卵巢功能依赖于一个复杂的血管系统的建立和持续重塑。这使卵泡和/或黄体(CL)能够接收所需的营养、氧气和激素支持,以及促进类固醇的释放。此外,血管生成的抑制导致卵泡生长减弱、排卵中断以及对 CL 的发育和功能产生严重影响。似乎血管内皮生长因子 A(VEGFA)的产生和作用在所有这些发育阶段都是必要的。然而,牛的成纤维细胞生长因子 2(FGF2)的表达比 VEGFA 更具动态性,在卵泡黄体转化期间急剧上调。这种上调很可能在高 VEGFA 水平存在的情况下引发强烈的血管生成。最近,我们开发了一种新的卵巢生理性血管生成培养系统,其中形成了高度组织化和复杂的内皮细胞网络。该系统将使我们能够阐明 FGF2 和 VEGFA 以及其他血管生成因子在黄体血管生成调节中的复杂相互作用。此外,最近的证据表明,周细胞可能在驱动血管生成中发挥积极作用,并强调了周细胞-内皮细胞相互作用在这一过程中的重要性。最后,有针对性地促进血管生成可能会导致开发新的策略来缓解黄体功能不足和不孕。

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