Profiling of Selected MicroRNAs in Proliferative Eutopic Endometrium of Women with Ovarian Endometriosis

Author:

Laudanski P.1,Charkiewicz R.2,Tolwinska A.3,Szamatowicz J.4,Charkiewicz A.5,Niklinski J.2

Affiliation:

1. Department of Perinatology, Medical University of Bialystok, Ulica Marii Sklodowskiej-Curie 24a, 15-276 Bialystok, Poland

2. Department of Clinical Molecular Biology, Medical University of Bialystok, Ul. Waszyngtona 13, 15-269 Bialystok, Poland

3. Clinic “EDMED” Białystok, Ul. Piasta 14, 15-044 Bialystok, Poland

4. Department of Gynecology and Gynecological Oncology, Medical University of Bialystok, Ulica Marii Sklodowskiej-Curie 24a, 15-276 Bialystok, Poland

5. Department of Medical Pathomorphology, Medical University of Bialystok, Ul. Waszyngtona 13, 15-269 Bialystok, Poland

Abstract

It has been well documented that aberrant expression of selected microRNAs (miRNAs) might contribute to the pathogenesis of disease. The aim of the present study is to compare miRNA expression by the most comprehensive locked-nucleic acid (LNA) miRNA microarray in eutopic endometrium of patients with endometriosis and control. In the study we recruited 21 patients with endometriosis and 25 were disease-free women. The miRNA expression profiles were determined using the LNA miRNA microarray and validated for selected molecules by real-time PCR. We identified 1198 human miRNAs significantly differentially altered in endometriosis versus control samples using false discovery rate of <5%. However only 136 miRNAs showed differential regulation by fold change of at least 1.3. By the use of selected statistical analysis we obtained 45 potential pathways that might play a role in the pathogenesis of endometriosis. We also found that natural killer cell mediated cytotoxicity pathway was found to be inhibited which is consistent with previous studies. There are several pathways that may be potentially dysregulated, due to abnormal miRNA expression, in eutopic endometrium of patients with endometriosis and in this way contribute to its pathogenesis.

Publisher

Hindawi Limited

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine

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