Effects of noncavity-distorting fibroids on endometrial gene expression and function†

Lusine Aghajanova, Sahar Houshdaran, Juan C. Irwin, Linda C. Giudice
In: Biology of Reproduction · 2017 · vol. 97(4) , pp. 564–576 · doi:10.1093/biolre/iox107 · PMID:29025102 · W2750999080
article OA: bronze CC0 ⤵ 8 in-corpus citations
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This study found that noncavity-distorting fibroids altered endometrial gene expression but did not affect tissue-level receptivity or decidualization markers, though stromal cells showed decreased proliferation and increased apoptosis.

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Abstract

Uterine fibroids are a common finding in infertility patients. Impaired implantation and decidualization have been proposed to contribute to compromised fertility. Data are limited on the endometrial transcriptome from subjects with uterine fibroids, as well as endometrial receptivity and decidualization potential of endometrial stromal fibroblasts (eSF) from women with fibroids. Our objective was to investigate the endometrial transcriptome of women with noncavity-distorting intramural fibroids and compare them to control subjects with no uterine pathology throughout the menstrual cycle. We also evaluated endometrial receptivity gene expression and basic endometrial functions such as decidualization, proliferation, and apoptosis in women with fibroid uterus. Results showed that large numbers of transcripts were significantly dysregulated throughout the menstrual cycle in fibroid subjects compared to controls. However, there were essentially no differences in the expression of receptivity markers at the tissue level, as well as decidualization markers in tissue and eSF in subjects with fibroids compared to controls. However, eSF from women with a fibroid uterus exhibited decreased proliferation potential and increased apoptosis upon decidualization. These data indicate preserved implantation and decidualization potential despite observed gene expression changes in endometrium from women with noncavity-distorting fibroids compared to controls. How this phenomenon and altered proliferation/apoptosis may contribute to impairment of endometrial function in subfertile patients warrants further investigation.

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