Increased expression of fibroblast growth factor receptor 1 in endometriosis and its correlation with endometriosis-related dysmenorrhea and recurrence
This study aims to identify a critical molecule that potentially participates in endometriosis pathogenesis and characterize its correlation with dysmenorrhea and recurrence. We utilized a bioinformatics-based strategy to screen for candidate genes and fibroblast growth factor receptor 1(FGFR1) was...
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Published in | European journal of obstetrics & gynecology and reproductive biology Vol. 184; pp. 117 - 124 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Ireland
Elsevier Ireland Ltd
01.01.2015
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Subjects | |
Online Access | Get full text |
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Summary: | This study aims to identify a critical molecule that potentially participates in endometriosis pathogenesis and characterize its correlation with dysmenorrhea and recurrence.
We utilized a bioinformatics-based strategy to screen for candidate genes and fibroblast growth factor receptor 1(FGFR1) was chosen for further validation. FGFR1 expression was examined in specimens of ectopic and eutopic endometrium obtained from 48 patients with endometriosis and specimens of eutopic endometrium from 26 healthy control subjects using immunohistochemistry and Western blotting. In addition, FGFR shRNA treatment was applied in a nude mice endometriosis model to examine the functional role of FGFR1 in endometriosis formation in vivo.
FGFR1 was found commonly overexpressed in ectopic endometrium of endometriosis compared with either its eutopic counterpart or endometrium from normal patients (P<0.05). FGFR shRNA treatment impaired endometriosis formation and alleviated endometriosis-related symptoms in vivo. FGFR1 expression in ectopic endometrium was correlated with dysmenorrhea severity (P<0.05) and recurrence in endometriosis patients (P<0.05).
FGFR1 might be involved in endometriosis development, which could possibly serve as a novel therapeutic target and prognostic marker for this disease. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0301-2115 1872-7654 1872-7654 |
DOI: | 10.1016/j.ejogrb.2014.11.013 |