Difference in expression of collagen type I and matrix metalloproteinase-1 in uterosacral ligaments of women with and without pelvic organ prolapse

Vulić, Marko; Strinić, Tomislav; Tomić, Snježana; Čapkun, Vesna; Jakus, Ivana Alujević; Stipic, Ivica

doi:10.1016/j.ejogrb.2010.12.019

Cited by 45 publications

(52 citation statements)

References 21 publications

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“…These results are consistent with the finding of others showing that POP has a statistically significant association with a moderate collagen III decrease. 8,27 Published data on collagen III expression associated with POP are inconsistent. These differences are likely due to measurement techniques since most studies relied on qualitative methodologies such as immunostaining or imaging.…”

Section: Discussionmentioning

confidence: 98%

Biomechanical Properties and Associated Collagen Composition in Vaginal Tissue of Women with Pelvic Organ Prolapse

Lee

Wen

et al. 2012

Journal of Urology

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Section: Discussionmentioning

confidence: 98%

Biomechanical Properties and Associated Collagen Composition in Vaginal Tissue of Women with Pelvic Organ Prolapse

Lee

Wen

et al. 2012

Journal of Urology

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“…Collagen type I (COL1) strengthens the connective tissues, whereas collagen type III (COL3) and elastin contribute to flexibility (9). Precursor collagens (COL1A1 and COL3A1) and elastin are synthesized by fibroblasts, and are then secreted into the ECM as the raw material of fibril assembly (6,22–24). The degradation of collagens depends on the activity of the interstitial matrix metalloproteinases (MMPs).…”

Section: Introductionmentioning

confidence: 99%

Role of transforming growth factor β-1 in the pathogenesis of pelvic organ prolapse: A potential therapeutic target

Liu

Wang

et al. 2017

International Journal of Molecular Medicine

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The present study aimed to reveal the metabolic alterations of the extracellular matrix (ECM) in uterosacral ligament (USL) with pelvic organ prolapse (POP) and to explore the role of transforming growth factor-β1 (TGF-β1) in pathogenesis of POP. For this purpse, 60 participants who underwent hysterectomy for benign indications were enrolled, 30 of which had symptomatic POP (grade II, III or IV) and composed the POP group, and the other 30 had asymptomatic POP (grade I or less) and served as the controls. Collagen fibers, elastin, matrix metalloproteinase (MMP)-2/9, tissue inhibitor of matrix metalloproteinases (TIMP)-2 and TGF-β1 were examined by Masson's trichrome staining, immunohistochemistry and RT-qPCR using USL biopsies. In vitro, human USL fibroblasts (hUSLFs) were primary cultured, pre-treated with recombinant TGF-β1 (0, 5, or 10 ng/ml) and then subjected to cyclic mechanical stretching (CMS; 0 or 5,333 με strain). Changes in the expression levels of collagen type I/III, elastin, TIMP-2, MMP-2/9 and Smad were detected. Our results revealed that at the tissue level, the expression of collagen fibers, elastin, TIMP-2 and TGF-β1 was significantly reduced in the POP group, while the activities of MMP-2/9 were significantly upregulated, compared with the control group. Statistical analysis indicated that the mRNA expression of TGF-β1 inversely correlated with the severity of POP partially. Our in vitro experimental data demonstrated that a CMS of 5333 με strain promoted the degradation of ECM proteins, inhibited the synthesis of TIMP-2, and upregulated the proteolytic activities of MMP-2/9. Pre-treatment with TGF-β1 attenuated the loss of ECM by stimulating the synthesis of TIMP-2 and inhibiting the activities of MMP-2/9 through the TGF-β1/Smad3 signaling pathway. On the whole, our data indicate that the reduced anabolism and increased catabolism of ECM proteins in USL are the pathological characteristics of POP. TGF-β1 not only has a specific value in predicting the severity of POP, but should also be considered as a novel therapeutic target for POP.

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“…[20][21][22] Several studies have compared the amount of total and individual subtypes of collagen in the supporting ligaments and vaginal tissue of women with POP to a control group (see Table 1). 19,[23][24][25][26][27][28][29][30][31][32][33][34][35][36] Figure 1 Current anatomical considerations for prolapse. Level 1: The upper 1/3 of the vagina is suspended to the pelvic wall by the uterosacral and cardinal ligaments, condensations of endopelvic fascia.…”

Section: Collagen Compositionmentioning

confidence: 99%

Recent studies of genetic dysfunction in pelvic organ prolapse: The role of collagen defects

Lim

Khoo

Wong

et al. 2014

Aust NZ J Obst Gynaeco

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Gynaecologists are becoming increasingly aware that women with a family history of prolapse are at an increased risk of prolapse refractory to treatment. In the past five years, several genetic mutations have been shown to correlate with increased prolapse susceptibility. These mutations can result in disordered collagen metabolism, which weaken the fascial support of the pelvic organs. This review examines the contemporary evidence regarding the role of collagen in prolapse.

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Difference in expression of collagen type I and matrix metalloproteinase-1 in uterosacral ligaments of women with and without pelvic organ prolapse

Cited by 45 publications

References 21 publications

Biomechanical Properties and Associated Collagen Composition in Vaginal Tissue of Women with Pelvic Organ Prolapse

Biomechanical Properties and Associated Collagen Composition in Vaginal Tissue of Women with Pelvic Organ Prolapse

Role of transforming growth factor β-1 in the pathogenesis of pelvic organ prolapse: A potential therapeutic target

Recent studies of genetic dysfunction in pelvic organ prolapse: The role of collagen defects

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