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Integrated Eutopic Endometrium and Non-Depleted Serum Quantitative Proteomic Analysis Identifies Candidate Serological Markers of Endometriosis

Manousopoulou A, Hamdan M, Fotopoulos M, Garay-Baquero DJ, Teng J, Garbis SD, et al.

Proteomics Clin Appl, 2019 05;13(3):e1800153.
PMID: 30488576 DOI: 10.1002/prca.201800153

BACKGROUND: Endometriosis affects about 4% of women in the reproductive age and is associated with subfertility. The aim of the present study is to examine the integrated quantitative proteomic profile of eutopic endometrium and serum from women with endometriosis compared to controls in order to identify candidate disease-specific serological markers.
METHODS: Eutopic endometrium and serum from patients with endometriosis (n = 8 for tissue and n = 4 for serum) are, respectively, compared to endometrium and serum from females without endometriosis (n = 8 for tissue and n = 4 for serum) using a shotgun quantitative proteomics method. All study participants are at the proliferative phase of their menstrual cycle.
RESULTS: At the tissue and serum level, 1214 and 404 proteins are differentially expressed (DEPs) in eutopic endometrium and serum, respectively, of women with endometriosis versus controls. Gene ontology analysis shows that terms related to immune response/inflammation, cell adhesion/migration, and blood coagulation are significantly enriched in the DEPs of eutopic endometrium, as well as serum. Twenty-one DEPs have the same trend of differential expression in both matrices and can be further examined as potential disease- and tissue-specific serological markers of endometriosis.
CONCLUSIONS: The present integrated proteomic profiling of eutopic endometrium and serum from women with endometriosis identify promising serological markers that can be further validated in larger cohorts for the minimally invasive diagnosis of endometriosis.

Matched MeSH terms: Endometriosis/pathology
Dissemination of endometrial cells at laparoscopy and chromotubation--a preliminary report

Kulenthran A, Jeyalakshmi N

Int. J. Fertil., 1989 Jul-Aug;34(4):256-8.
PMID: 2570762

Twenty-one patients undergoing laparoscopy and chromotubation were investigated for the dissemination of endometrial cells into the pelvic cavity. Prechromotubation fluid and postchromotubation fluid from the posterior cul-de-sac were aspirated and subjected to cytological assessment. Four patients (15.4%) showed evidence of endometrial cell dissemination into the pelvic cavity.

Matched MeSH terms: Endometriosis/pathology*
Scar endometriosis presenting as an acute abdomen: a case report

Khoo JJ

Aust N Z J Obstet Gynaecol, 2003 Apr;43(2):164-5.
PMID: 14712976
Matched MeSH terms: Endometriosis/pathology
Fulltext The sensitivity of the DNA damage checkpoint prevents oocyte maturation in endometriosis

Hamdan M, Jones KT, Cheong Y, Lane SI

Sci Rep, 2016 11 14;6:36994.
PMID: 27841311 DOI: 10.1038/srep36994

Mouse oocytes respond to DNA damage by arresting in meiosis I through activity of the Spindle Assembly Checkpoint (SAC) and DNA Damage Response (DDR) pathways. It is currently not known if DNA damage is the primary trigger for arrest, or if the pathway is sensitive to levels of DNA damage experienced physiologically. Here, using follicular fluid from patients with the disease endometriosis, which affects 10% of women and is associated with reduced fertility, we find raised levels of Reactive Oxygen Species (ROS), which generate DNA damage and turn on the DDR-SAC pathway. Only follicular fluid from patients with endometriosis, and not controls, produced ROS and damaged DNA in the oocyte. This activated ATM kinase, leading to SAC mediated metaphase I arrest. Completion of meiosis I could be restored by ROS scavengers, showing this is the primary trigger for arrest and offering a novel clinical therapeutic treatment. This study establishes a clinical relevance to the DDR induced SAC in oocytes. It helps explain how oocytes respond to a highly prevalent human disease and the reduced fertility associated with endometriosis.

Matched MeSH terms: Endometriosis/pathology*