摘要
Abstract (Summary)Infertility in females is the inability to become and maintain pregnancy, which can be caused by the abnormal development of a corpus luteum (CL). Abnormal development is linked to incomplete angiogenesis, which leads to an overall decrease in progesterone production. Angiogenesis is regulated by factors, such as fibroblast growth factor-2 (FGF-2), vascular endothelial growth factor (VEGF), and angiopoietin-1 (Ang-1) all of which are expressed in developing luteal tissue. Leptin, a potent satiety hormone, influences the expression of FGF and VEGF in non-ovarian tissue, and is also produced in the CL. Hence, it is hypothesized that leptin influences the production of FGF-2, VEGF, and Ang-1 in the developing CL. The objectives of the study were to (1) characterize angiogenic factor expression in the developing porcine CL and (2) determine the effect of leptin on FGF-2, VEGF, and Ang-1 expression in dispersed luteal tissue. Thirty mature crossbred gilts of similar age were allocated to one of five treatments (days of CL development: d 3, 4, 5, 6, or 7 of the estrous cycle; n=6/day) for tissue collection. Gilts were checked twice daily for classical, behavioral estrus using a boar for detection. Blood samples were collected on the day of CL harvest for serum progesterone analysis. Luteal tissue was divided and either embedded for immunohistochemistry, frozen in liquid nitrogen, or enzymatically digested and dispersed for culture. Dispersed cells were cultured with or without leptin (0, 10 -12 , 10 -11 , 10 -10 , 10 -9 , 10 -8 M; n = 3 wells/dose/gilt) for 24 hrs. Total expression for VEGF, FGF-2, Ang-1, and the leptin receptor (OB-Rb) was determined in all samples. All angiogenic factors and OB-Rb were localized to vascular endothelial cells, small luteal cells and large luteal cells; however, concentration and predominant cellular location varied by day of development. The expression of FGF-2 was highest (P = 0.05) on day 6 and leptin increased linearly (P = 0.005) as the CL developed. Leptin dose dependently decreased (P ≤ 0.05) VEGF, FGF-2 and Ang-1, relative to day of luteal development, by 10, 17 and 16.8%, respectively. Therefore, leptin appears to be involved in the angiogenic process in developing CL tissue.
摘要译文
抽象（摘要）不育女性是无法成为和维持妊娠，这可以通过一个黄体（CL）的发育异常而引起。发育异常被链接到不完全的血管生成，这导致在孕酮生产整体减少。所有这些血管生成被因子，如成纤维细胞生长因子-2（FGF-2），血管内皮生长因子（VEGF），和血管生成素-1上调（的Ang-1）表示在显影黄体组织。瘦素，一种有效的饱腹感激素，影响FGF和VEGF在非卵巢组织的表达，并且也产生在CL。因此，可以推测，瘦素影响的FGF-2的，VEGF和Ang-1的生产在显影CL上。这项研究的目的是（1）在显影猪CL表征血管生成因子的表达和（2）确定瘦素对FGF-2的效果，在分散的黄体组织的VEGF，和Ang-1的表达。类似年龄的三十成熟杂交母猪被分配到五个处理之一（CL发展的天数：d 3处，4，5，6，或发情周期的7; N = 6 /天）组织采集。小母猪每天两次用公猪检测古典，行为发情检查。采集血样CL上收获的一天血清孕酮分析。黄体组织分割，要么嵌入用于免疫组织化学，在液氮中冷冻，或酶促消化并分散培养。分散的细胞进行培养有或没有瘦素（0，10 -12，10 -11，10 -10，10 -9，10 -8 M; n = 3的孔/剂量/镀金）24小时。总表达对VEGF，FGF-2，的Ang-1，和瘦蛋白受体（OB-Rb的）中的所有样品中确定。所有血管生成因子和OB-Rb的分别定位于血管内皮细胞，小黄体细胞和大黄体细胞;然而，浓度和主要的细胞定位由不同的发展一天。FGF-2的表达最高（P = 0.05）在第6天，瘦素线性增加（P = 0.005）作为CL开发。瘦素剂量依赖性降低（P＆乐; 0.05），VEGF，FGF-2和Ang-1，相对于黄体发展的一天，由分别为10，17和16.8％25。因此，瘦素似乎参与在显影CL组织血管生成过程。