Early endometriosis invades the extracellular matrix
Observational
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⤵ 119 in-corpus citations
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Aminoterminal propeptide of type III procollagen was elevated in peritoneal fluid of women with early endometriosis, indicating active extracellular matrix invasion.
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Abstract
OBJECTIVES: To investigate whether the aminoterminal propeptides of type III procollagen are increased in patients with early endometriosis and to demonstrate that the subtle lesion of endometriosis is an active stage of the disease.
DESIGN: Aminoterminal propeptide of type III procollagen was determined in serum and peritoneal fluid (PF) of 100 consecutive patients undergoing laparoscopy.
SETTING: Academisch Ziekenhuis Maastricht, The Netherlands, a tertiary care center.
RESULTS: Aminoterminal propeptide PF levels were significantly higher in women with early lesions of endometriosis compared with levels in two groups of controls, i.e., fertile, cycling, women without the disease (P = 0.019) and women on oral contraceptives without the disease (P = 0.036). No difference was found in aminoterminal propeptide PF levels when comparing patients with early lesions of endometriosis and patients with unexplained infertility, the third control group. Aminoterminal propeptide PF levels of patients with endometriosis without early lesions were not different from PF levels in controls.
CONCLUSION: The early lesion is an active stage of endometriosis, invading the extracellular matrix. In women with unexplained infertility active, microscopic endometriosis may be present.
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- Curcumin and Endometriosis 2020
- The Pathogenesis of Endometriosis: Molecular and Cell Biology Insights 2019
- Melatonin Promotes Uterine and Placental Health: Potential Molecular Mechanisms 2019
- Polychlorinated biphenyl 104 promotes migration of endometrial stromal cells in endometriosis 2018
- Identifying biomarkers for non-invasive diagnosis of endometriosis 2016
- Leptin promotes human endometriotic cell migration and invasion by up-regulating MMP-2 through the JAK2/STAT3 signaling pathway 2015
- Molecular aspects of endometriosis 2015
- Melatonin and genital endometriosis - new possibilities of therapy 2015
- Hypoxia Promotes Invasion of Endometrial Stromal Cells via Hypoxia-Inducible Factor 1α Upregulation-Mediated β-Catenin Activation in Endometriosis 2015
- Genetic variation of the E-cadherin gene is associated with primary infertility in patients with ovarian endometriosis 2014
- Understanding the role of epigenomic, genomic and genetic alterations in the development of endometriosis (review) 2014
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- Endometriosis: Disease Classification and Behavior 2011
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- Abnormal regulation of chemokine TECK and its receptor CCR9 in the endometriotic milieu is involved in pathogenesis of endometriosis by way of enhancing invasiveness of endometrial stromal cells 2010
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- Altered expression of claudin-3 and claudin-4 in ectopic endometrium of women with endometriosis 2008
- Matrix metalloproteinases 2 and 9, E-cadherin, and beta-catenin expression in endometriosis, low-grade endometrial carcinoma and non-neoplastic eutopic endometrium 2008
- Role of melatonin in regulating matrix metalloproteinase-9 via tissue inhibitors of metalloproteinase-1 during protection against endometriosis 2008
- Association of three single nucleotide polymorphisms of the E-cadherin gene with endometriosis in a Chinese population 2007
- Detection of endometriosis with the use of plasma protein profiling by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry 2007
- Gene expression profiles and functional characterization of human immortalized endometriotic epithelial and stromal cells 2007
- Trichostatin A, a histone deacetylase inhibitor, attenuates invasiveness and reactivates E-cadherin expression in immortalized endometriotic cells 2007
- Endometrial cells from women with endometriosis have increased adhesion and proliferative capacity in response to extracellular matrix components: towards a mechanistic model for endometriosis progression 2007
- Nuclear factor-kappab (NF-kappaB): an unsuspected major culprit in the pathogenesis of endometriosis that is still at large? 2006
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