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Proteomics of Uterosacral Ligament Connective Tissue from Women with and without Pelvic Organ Prolapse
Author(s) -
Li XiangJuan,
Pan HaiTao,
Chen JuanJuan,
Fu YiBin,
Fang Min,
He GuoHua,
Zhang Tao,
Ding HaiGang,
Yu Bin,
Cheng Yi,
Tan YaJing,
Zhao FaLin,
Morse Abraham N.,
Huang HeFeng
Publication year - 2019
Publication title -
proteomics – clinical applications
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.948
H-Index - 54
eISSN - 1862-8354
pISSN - 1862-8346
DOI - 10.1002/prca.201800086
Subject(s) - uterosacral ligament , connective tissue , medicine , pathogenesis , tenascin , pathology , anatomy , biology , microbiology and biotechnology , vagina , extracellular matrix , fibronectin
Purpose Damage to the uterosacral ligaments is an important contributor to uterine and vaginal prolapse. The aim of this study is to identify differentially expressed proteins (DEPs) in the uterosacral ligaments of women with and without pelvic organ prolapse (POP) and analyze their relationships to cellular mechanisms involved in the pathogenesis of POP. Experimental design Uterosacral ligament connective tissue from four patients with POP and four control women undergo iTRAQ analysis followed by ingenuity pathway analysis (IPA) of DEPs. DEPs are validated using Western blot analysis. Results A total of 1789 unique protein sequences are identified in the uterosacral ligament connective tissues. The expression levels of 88 proteins are significantly different between prolapse and control groups (≥1.2‐fold, p < 0.05). IPA demonstrates the association of 14 DEPs with “Connective Tissue Function.” Among them, fibromodulin, collagen alpha‐1 (XIV) chain, calponin‐1, tenascin, and galectin‐1 appear most likely to play a role in the etiology of POP. Conclusions and clinical relevance At least six proteins not previously associated with the pathogenesis of POP with biologic functions that suggest a plausible relationship to the disorder are identified. These results may be helpful for furthering the understanding of the pathophysiological mechanisms of POP.