PTH缺乏经细胞外钙介导卵巢血管生成障碍而致生殖能力降低  

Parathyroid hormone deficiency resulted in fertility defects mediated through extracellular calcium

作　　者：郭健[1] 苗登顺[1] 

机构地区：[1]南京医科大学人体解剖学系,江苏南京210029

出　　处：《南京医科大学学报（自然科学版）》2009年第5期628-633,共6页Journal of Nanjing Medical University(Natural Sciences)

摘　　要：目的:探讨甲状旁腺素(PTH)缺乏引起生殖功能降低的机制。方法:使用组织学,免疫组织化学和Westernblot的方法比较分析了同窝4个月PTH基因敲除纯合子小鼠和野生型小鼠分别给予正常钙(1%)、低钙(0.01%)及高钙饮食(2%)后生殖能力、卵巢成熟卵泡数量、黄体形成及血管生成的差异。结果:与同窝野生型雌性小鼠(PTH+/+)相比,正常饮食PTH基因敲除纯合子小鼠(PTH-/-)生殖能力下降,成熟卵泡数量及黄体生成减少,卵巢血管发生减少;低钙饮食PTH-/-表现为完全不孕,成熟卵泡数量进一步减少和黄体缺失,卵巢血管发生减少更为明显;而高钙饮食PTH-/-生殖能力、成熟卵泡数量、黄体形成及血管发生均恢复正常。结论:PTH缺乏经细胞外钙介导卵巢血管生成障碍而致生殖能力降低。Objective：To investigate the mechanism of the PTH deficiency resulting in fertility defects in female mice. Methods： Capacity of fertility, the number of tertiary follicles, corpus luteum formation and angiogenesis were compared between PTH knock-out and wild-type littermates at 4 months of ages fed either on normal calcium（ 1%）,low calcium（0.01%） and high calcium（2%） diet by using histology,immunohistochemistry and Western-blot, respectively. Results： Compared with wild-type mice ,on the normal calcium diet, PTH knock-out mice displayed lower fertility capacity, decreased number of tertiary follicles and formation of corpus luetum and reduced the angiogenesis in ovary; On the low calcium diet,PTH knock-out mice displayed completely infertile,further decreased number of tertiary follicles without the corpus luteum formation and reduced angiogenesis in ovary more dramatically; Whereas on the high calcium diet, PTH knock-out mice were normalized for all fertility parameters including the number of tertiary follicles, the corpus luteum formation and angiogenesis in ovary. Conclusion：PTH deficiency resulted in fertility defects mediated through extracellular calcium.

关 键 词：PTH 基因敲除 不孕 饮食钙 血管发生 

分 类 号：Q573[生物学—生物化学]