Changes of glycoprotein and collagen immunolocalization in the uterine artery wall of postmenopausal women with and without pelvic organ prolapse

被引:13
作者
Goepel, Christian [1 ]
Kantelhardt, Eva Johanna [1 ]
Karbe, Ina [1 ]
Stoerer, Sandra [1 ]
Dittmer, Juergen [1 ]
机构
[1] Univ Halle Wittenberg, Dept Obstet & Gynecol, D-06097 Halle, Saale, Germany
关键词
Extracellular matrix; Uterine artery; Pelvic organ prolapse; Collagen; Glycoprotein; Elastin; Human; ELASTIN GENE-EXPRESSION; CONNECTIVE-TISSUE; EXTRACELLULAR-MATRIX; UTEROSACRAL LIGAMENTS; CARDINAL LIGAMENTS; TENASCIN; METABOLISM; RADIOIMMUNOASSAY; PROTEOGLYCANS; INCONTINENCE;
D O I
10.1016/j.acthis.2010.02.001
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Pelvic organ prolapse (POP) is accompanied by an altered composition of the extracellular matrix (ECM). However, it is unclear whether the changed ECM is the cause or the consequence of POP, as stretching of the tissue may have an effect on the composition of the ECM. To address this question, we analyzed the connective tissues of the uterine artery wall of postmenopausal women with and without POP. The uterine artery wall is stretched in patients with POP, but this stretching is unlikely to cause the POP. Twenty-one women (13 with POP and 8 without POP) hospitalized for hysterectomy were included in this study. Tissue samples from the uterine artery were analyzed for collagen (types I, III, IV, V and VI) and other ECM proteins (fibronectin, laminin, tenascin, vitronectin and elastin) using immunofluorescence microscopy. Results revealed that uterine artery samples of women with prolapse showed a significantly weaker immunoreactivity to type VI collagen, vitronectin and elastin and a stronger immunostaining for type III collagen and tenascin as compared to control samples. Our results suggest that the ECM may be altered in response to mechanical stretch. Changes in the ECM composition as observed in POP may not necessarily be the reason for the development of pelvic floor relaxation in postmenopausal women (C) 2010 Elsevier GmbH. All rights reserved.
引用
收藏
页码:375 / 381
页数:7
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