Collagen metabolism and turnover in women with stress urinary incontience and pelvic prolapse
Collagen metabolism and turnover in women with stress urinary incontience and pelvic prolapse
复制标题
DOI：
10.1007/s001920200020
复制
发表时间：
2002-04-01
影响因子：
1.8
通讯作者：
Polan, ML
中科院分区：
文献类型：
--
作者：
Chen, BH;Wen, Y;Polan, ML
本研究的目的是探讨定量mRNA表达的基质金属蛋白酶MMP-1，MMP-2，MMP-9，及其抑制剂，金属蛋白酶组织抑制剂TIMP-1，TIMP-2和TIMP-3，在阴道壁组织中的女性压力性尿失禁相比，大陆控制。阴道壁组织来自7名患有压力性尿失禁/严重盆腔脱垂的女性和15名对照组。然后提取RNA并定量。用寡核苷酸引物进行定量竞争性逆转录（QC-RT-PCR）以定量MMP-1、MMP-2、MMP-9、TIMP-1、TIMP-2和TIMP-3 mRNA的表达。压力控制组TIMP-I及mRNA表达水平显著降低（P = 0.03）。TIMP-2、TIMP-3、MMP-2、MMP-9 mRNA表达在应激性尿失禁组与对照组之间无差异。然而，在失禁组中MMP-1 mRNA表达显著增加（P = 0.05），并且MMP-1/TIMP-1比率（P = 0.04）与压力性尿失禁中胶原降解增加一致。应激性尿失禁妇女表现出MMP-1 mRNA表达的增加和抑制剂TIMP-1 mRNA表达的减少。这两个结果是一致的增加胶原蛋白分解作为一种病理病因的尿失禁。
The aim of this study was to investigate quantitative mRNA expression of matrix metalloproteinases MMP-1, MMP-2, MMP-9, and their inhibitors, the tissue inhibitors of metalloproteinases TIMP-1, TIMP-2 and TIMP-3, in vaginal wall tissue from women with stress urinary incontinence compared to continent controls. Vaginal wall tissues were obtained from 7 women with stress urinary incontinence/severe pelvic prolapse and 15 continent controls. RNA was then extracted and quantified. Quantitative competitive reverse transcription (QC-RT-PCR) was carried out with oligonucleotide primers to quantify MMP-1, MMP-2, MMP-9, TIMP-1, TIMP-2 and TIMP-3 mRNA expression. Stress continent women demonstrated a significant decrease in TIMP-I and mRNA expression (P = 0.03). There was no difference in TIMP-2, TIMP-3, MMP-2 or MMP-9 mRNA expression between stress incontinent women and controls. However, MMP-1 mRNA expression was significantly increased (P = 0.05) in the incontinent group and the MMP-1/TIMP-1 ratio (P = 0.04) was consistent with increased collagen degradation in the stress incontinence. Stress incontinent women demonstrated an increase in MMP-1 mRNA expression and a decrease in the inhibitor TIMP-1 mRNA expression. Both these findings are consistent with increased collagen breakdown as a pathologic etiology of incontinence.