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Expression changes in pelvic organ prolapse: a systematic review and in silico study

Pelvic organ prolapse (POP) is a highly disabling condition common for a vast number of women worldwide. To contribute to existing knowledge in POP pathogenesis, we performed a systematic review of expression studies on both specific gene and whole-genome/proteome levels and an in silico analysis of...

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Detalles Bibliográficos
Autores principales: Khadzhieva, Maryam B., Kolobkov, Dmitry S., Kamoeva, Svetlana V., Salnikova, Lyubov E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5550478/
https://www.ncbi.nlm.nih.gov/pubmed/28794464
http://dx.doi.org/10.1038/s41598-017-08185-6
Descripción
Sumario:Pelvic organ prolapse (POP) is a highly disabling condition common for a vast number of women worldwide. To contribute to existing knowledge in POP pathogenesis, we performed a systematic review of expression studies on both specific gene and whole-genome/proteome levels and an in silico analysis of publicly available datasets related to POP development. The most extensively investigated genes in individual studies were related to extracellular matrix (ECM) organization. Three premenopausal and two postmenopausal sets from two Gene Expression Omnibus (GEO) studies (GSE53868 and GSE12852) were analyzed; Gene Ontology (GO) terms related to tissue repair (locomotion, biological adhesion, immune processes and other) were enriched in all five datasets. Co-expression was higher in cases than in controls in three premenopausal sets. The shared between two or more datasets up-regulated genes were enriched with those related to inflammatory bowel disease (IBD) in the NHGRI GWAS Catalog. ECM-related genes were not over-represented among differently expressed genes. Up-regulation of genes related to tissue renewal probably reflects compensatory mechanisms aimed at repair of damaged tissue. Inefficiency of this process may have different origins including age-related deregulation of gene expression.