Proteolytic and cellular death mechanisms in ovulatory ovarian rupture.

W J Murdoch
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引用次数: 42

Abstract

Collagen breakdown and cellular death (apoptosis and inflammatory necrosis) within the apex of preovulatory ovine follicles are hallmarks of impending ovarian rupture. An integrative mechanism is presented whereby gonadotropic stimulation of urokinase-type plasminogen activator secretion by ovarian surface epithelial cells bordering the preovulatory follicle elicits a localized increase in tissue plasmin, which activates latent collagenases and secretion of tumor necrosis factor-alpha (TNF-alpha) from thecal endothelium. TNF-alpha potentiates collagenolysis (via matrix metalloproteinase gene expression) and (at elevated concentrations) mediates epithelial/vascular dissolution. Incidental damage to DNA of ovarian surface epithelial cells circumjacent to the ruptured follicle is a putative etiological factor in ovarian cancer.

排卵期卵巢破裂的蛋白水解和细胞死亡机制。
排卵前卵泡顶端的胶原蛋白分解和细胞死亡(细胞凋亡和炎症性坏死)是即将发生的卵巢破裂的标志。一个综合的机制提出,促性腺激素刺激尿激酶型纤溶酶原激活剂的分泌,卵巢表面上皮细胞与排卵前卵泡相邻,引起组织纤溶酶的局部增加,从而激活潜伏的胶原酶和肿瘤坏死因子- α (tnf - α)的分泌。tnf - α增强胶原溶解(通过基质金属蛋白酶基因表达)和(在浓度升高时)介导上皮/血管溶解。卵泡破裂周围卵巢表面上皮细胞DNA的偶然损伤被认为是卵巢癌的病因。
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