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      Collagen metabolic disorder induced by oxidative stress in human uterosacral ligament-derived fibroblasts: A possible pathophysiological mechanism in pelvic organ prolapse

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          Abstract

          Pelvic organ prolapse (POP) is a global health problem, for which the pathophysiological mechanism remains to be fully elucidated. The loss of extracellular matrix protein has been considered to be the most important molecular basis facilitating the development of POP. Oxidative stress (OS) is a well-recognized mechanism involved in fiber metabolic disorders. The present study aimed to clarify whether OS exists in the uterosacral ligament (USL) with POP, and to investigate the precise role of OS in collagen metabolism in human USL fibroblasts (hUSLFs). In the present study, 8-hydroxyguanosine (8-OHdG) and 4 hydroxynonenal (4-HNE), as oxidative biomarkers, were examined by immunohistochemistry to evaluate oxidative injury in USL sections in POP (n=20) and non-POP (n=20) groups. The primary cultured hUSLFs were treated with exogenous H 2O 2 to establish an original OS cell model, in which the expression levels of collagen, type 1, α1 (COL1A1), matrix metalloproteinase (MMP)-2, tissue inhibitor of metalloproteinase (TIMP)-2 and transforming growth factor (TGF)-β1 were evaluated by western blot and reverse transcription-quantitative polymerase chain reaction analyses. The results showed that the expression levels of 8-OHdG and 4-HNE in the POP group were significantly higher, compared with those in the control group. Collagen metabolism was regulated by H 2O 2 exposure in a concentration-dependent manner, in which lower concentrations of H 2O 2 (0.1–0.2 mM) stimulated the anabolism of COL1A1, whereas a higher concentration (0.4 mM) promoted catabolism. The expression levels of MMP-2, TIMP-2 and TGF-β1 exhibited corresponding changes with the OS levels. These results suggested that OS may be involved in the pathophysiology of POP by contributing to collagen metabolic disorder in a severity-dependent manner in hUSLFs, possibly through the regulation of MMPs, TIMPs and TGF-β1 indirectly.

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          The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction.

          Richard C. Bump, Anders Mattiasson, Kari Bø … (1996)
          This article presents a standard system of terminology recently approved by the International Continence Society, the American Urogynecologic Society, and the Society of Gynecologic Surgeons for the description of female pelvic organ prolapse and pelvic floor dysfunction. An objective site-specific system for describing, quantitating, and staging pelvic support in women is included. It has been developed to enhance both clinical and academic communication regarding individual patients and populations of patients. Clinicians and researchers caring for women with pelvic organ prolapse and pelvic floor dysfunction are encouraged to learn and use the system.
          Article 0 comments Cited 531 times – based on 0 reviews     Review now
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            Pathophysiology of premature skin aging induced by ultraviolet light.

            G Fisher, Z. Wang, S Datta … (1997)
            Long-term exposure to ultraviolet irradiation from sunlight causes premature skin aging (photoaging), characterized in part by wrinkles, altered pigmentation, and loss of skin tone. Photoaged skin displays prominent alterations in the collagenous extracellular matrix of connective tissue. We investigated the role of matrix-degrading metalloproteinases, a family of proteolytic enzymes, as mediators of collagen damage in photoaging. We studied 59 whites (33 men and 26 women, ranging in age from 21 to 58 years) with light-to-moderate skin pigmentation, none of whom had current or prior skin disease. Only some of the participants were included in each of the studies. We irradiated their buttock skin with fluorescent ultraviolet lights under standard conditions and obtained skin samples from irradiated and nonirradiated areas by keratome or punch biopsy. In some studies, tretinoin and its vehicle were applied to skin under occlusion 48 hours before ultraviolet irradiation. The expression of matrix metalloproteinases was determined by in situ hybridization, immunohistology, and in situ zymography. Irradiation-induced degradation of skin collagen was measured by radioimmunoassay of soluble cross-linked telopeptides. The protein level of tissue inhibitor of matrix metalloproteinases type 1 was determined by Western blot analysis. A single exposure to ultraviolet irradiation increased the expression of three matrix metalloproteinases -- collagenase, a 92-kd gelatinase, and stromelysin -- in skin connective tissue and outer skin layers, as compared with nonirradiated skin. The degradation of endogenous type I collagen fibrils was increased by 58 percent in irradiated skin, as compared with nonirradiated skin. Collagenase and gelatinase activity remained maximally elevated (4.4 and 2.3 times, respectively) for seven days with four exposures to ultraviolet irradiation, delivered at two-day intervals, as compared with base-line levels. Pretreatment of skin with tretinoin (all-trans-retinoic acid) inhibited the induction of matrix metalloproteinase proteins and activity (by 70 to 80 percent) in both connective tissue and outer layers of irradiated skin. Ultraviolet irradiation also induced tissue inhibitor of matrix metalloproteinases-1, which regulates the enzyme. Induction of the inhibitor was not affected by tretinoin. Multiple exposures to ultraviolet irradiation lead to sustained elevations of matrix metalloproteinases that degrade skin collagen and may contribute to photoaging. Treatment with topical tretinoin inhibits irradiation-induced matrix metalloproteinases but not their endogenous inhibitor.
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              Pelvic organ prolapse.

              J. Jelovsek, Christopher Maher, Linda Barber (2007)
              Pelvic organ prolapse is downward descent of female pelvic organs, including the bladder, uterus or post-hysterectomy vaginal cuff, and the small or large bowel, resulting in protrusion of the vagina, uterus, or both. Prolapse development is multifactorial, with vaginal child birth, advancing age, and increasing body-mass index as the most consistent risk factors. Vaginal delivery, hysterectomy, chronic straining, normal ageing, and abnormalities of connective tissue or connective-tissue repair predispose some women to disruption, stretching, or dysfunction of the levator ani complex, connective-tissue attachments of the vagina, or both, resulting in prolapse. Patients generally present with several complaints, including bladder, bowel, and pelvic symptoms; however, with the exception of vaginal bulging, none is specific to prolapse. Women with symptoms suggestive of prolapse should undergo a pelvic examination and medical history check. Radiographic assessment is usually unnecessary. Many women with pelvic organ prolapse are asymptomatic and do not need treatment. When prolapse is symptomatic, options include observation, pessary use, and surgery. Surgical strategies for prolapse can be categorised broadly by reconstructive and obliterative techniques. Reconstructive procedures can be done by either an abdominal or vaginal approach. Although no effective prevention strategy for prolapse has been identified, considerations include weight loss, reduction of heavy lifting, treatment of constipation, modification or reduction of obstetric risk factors, and pelvic-floor physical therapy.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mol Med Rep
                Journal ID (iso-abbrev): Mol Med Rep
                Title: Molecular Medicine Reports
                Publisher: D.A. Spandidos
                ISSN (Print): 1791-2997
                ISSN (Electronic): 1791-3004
                Publication date (Print): April 2016
                Publication date (Electronic): 22 February 2016
                Publication date PMC-release: 22 February 2016
                Volume: 13
                Issue: 4
                Pages: 2999-3008
                Affiliations
                Department of Gynecology and Obstetrics, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China
                Author notes
                Correspondence to: Dr Li Hong, Department of Gynecology and Obstetrics, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan, Hubei 430060, P.R. China, E-mail: 2013103020057@ 123456whu.edu.cn
                [*]

                Contributed equally

                Article
                Publisher ID: mmr-13-04-2999
                DOI: 10.3892/mmr.2016.4919
                PMC ID: 4805094
                PubMed ID: 26936098
                SO-VID: eaff4933-b45d-4f81-9284-ae6ff86d5515
                Copyright © Copyright: © Liu et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 18 March 2015
                Date accepted : 20 January 2016
                Categories
                Subject: Articles

                Keywords: pelvic organ prolapse,oxidative stress,tissue inhibitor of metalloproteinase,matrix metalloproteinase,collagen metabolism,transforming growth factor-β1
                Data availability:
                Keywords: pelvic organ prolapse, oxidative stress, tissue inhibitor of metalloproteinase, matrix metalloproteinase, collagen metabolism, transforming growth factor-β1

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