MicroRNA expression profile in endometriosis: its relation to angiogenesis and fibrinolytic factors

Braza-Boïls, Aitana; Marí-Alexandre, Josep; Gilabert, J.; Sánchez-Izquierdo, Dolors; España, Francisco; Estellés, Amparo; Gilabert-Estellés, Juan

doi:10.1093/humrep/deu019

Cited by 132 publications

(100 citation statements)

References 56 publications

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“…Despite extensive research, the pathogenesis of endometriosis remains unclear because it is complex. Recently, several studies have revealed that aberrant miRNA profiles are correlated with endometriosis (Ohlsson Teague et al, 2009;Braza-Boïls et al, 2014;Rekker et al, 2015). In particular, our own and previous studies indicated that members of the miR-200 family (miR-200a, miR-200b, and miR-200c) were downregulated in endometriosis-associated tissues (Ohlsson Teague et al, 2009;Braza-Boïls et al, 2014;Rekker et al, 2015).…”

Section: Discussionmentioning

confidence: 85%

Microarray analysis of microRNA deregulation and angiogenesis-related proteins in endometriosis

Teng

et al. 2016

Genet. Mol. Res.

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ABSTRACT. We examined the aberrant microRNA (miRNA) expression profile responsible for the changes in angiogenesis observed in endometriotic lesions. This study revealed characteristic miRNA expression profiles associated with endometriosis in endometrial tissue and endometriotic lesions from the same patient, and their correlation with the most important angiogenic and fibrinolytic factors. miRNA expression was quantified using a microRNA array and reversetranscription microRNA polymerase chain reaction. Levels of vascular endothelial growth factor A (VEGFA), epidermal growth factor receptor 2 (EGFR2), phosphatase and tensin homolog (PTEN), and C-X-C chemokine receptor type 4 (CXCR4) were quantified using enzyme-linked immunosorbent assay. The endometrial tissue showed significantly lower levels of miR-200b, miR-15a-5p, miR-19b-1-5p, miR-146a-5p, and miR-200c, and higher levels of miR-16-5p, miR106b-5p, and miR-145-5p. VEGFA was significantly upregulated, whereas EGFR2, PTEN, and CXCR4 were markedly downregulated, in the endometriotic tissues compared to that in the normal endometrial tissues. In conclusion, differences in the miRNA levels could modulate the expression of VEGFA, EGFR2, PTEN, and CXCR4, and may play an important role in the pathogenesis of endometriosis. The higher angiogenic and proteolytic activities observed in the eutopic endometrium might facilitate the implantation of endometrial cells at ectopic sites.

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Section: Discussionmentioning

confidence: 85%

Microarray analysis of microRNA deregulation and angiogenesis-related proteins in endometriosis

Teng

et al. 2016

Genet. Mol. Res.

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“…It has been reported that certain miRs, including miR-191, miR-142-3p, miR-29c and miR-210, serve important roles in endometriosis (23,24). The pathogenesis of AM and endometriosis are similar as they both result from the invasion and metastasis of endometrial cells (25)(26)(27). Therefore, it was speculated that miRs may also be involved in AM.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-17 downregulates expression of the PTEN gene to promote the occurrence and development of adenomyosis

2017

Experimental and Therapeutic Medicine

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Abstract. The aim of the current study was to evaluate the expression of microRNA (miR)-17 in the endometrial tissues of patients with adenomyosis (AM) and determine its biological function in the occurrence and development of the disease. A total of 45 fresh endometrial tissues of AM patients and 32 normal endometrial tissues were collected from healthy controls. The expression of miR-17 was evaluated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The miR-17-targeting gene phosphatase and tensin homolog (PTEN) was predicted using bioinformatics and its expression was evaluated with RT-qPCR and western blot analysis. Endometrial cells were isolated from patients with AM and healthy controls. They were cultured in vitro and transfected with antagomiR-17 to downregulate miR-17 expression, subsequently cell viability and apoptosis were measured using MTT and flow cytometry. The expression of PTEN and cell cycle-and apoptosis-related proteins were evaluated using western blot analysis. Endometrial cells that stably overexpressed PTEN were screened in vitro by co-culture with G418. A dual-luciferase reporter assay was conducted to verify whether miR-17 was directly bound to PTEN mRNA. The results demonstrated that expression of miR-17 was significantly increased in the endometrial tissues of patients with AM compared with control patients (P<0.05). PTEN mRNA and protein expression were significantly lower in the AM group compared with the control group (P<0.05). When the expression of miR-17 in the cells was downregulated, the expression of PTEN was significantly increased (P<0.05). In addition, expression of Bcl-2 protein was significantly decreased and that of Bax protein significantly increased compared with the negative control (both P<0.05). The expression of cyclins E1 and D1 were also significantly downregulated (P<0.05). When PTEN was overexpressed or miR-17 was downregulated, the viability of endometrial cells significantly decreased and cell apoptosis significantly increased (all P<0.05). A dual-luciferase reporter assay indicated that miR-17 could directly bind to the PTEN mRNA 3'-untranslated region to regulate its expression. Thus the current study indicates that expression of miR-17 was increased in the endometrial tissues of patients with AM and may influence cell apoptosis and cyclin expression through the targeted regulation of PTEN. These results suggest that miR-17 promotes the occurrence and development of AM.

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“…An emerging field in endometriosis is the function of miRNA in angiogenesis. Primary eutopic and ectopic endometrial stromal cells exposed to PF from women with endometriosis have downregulated miRNAs known to regulate VEGF expression compared to cells exposed to PF from control women (Braza-Boils et al 2013, Braza-Boils et al 2014, Braza-Boils et al 2015). Future in-depth analysis of the interplay between inflammation and angiogenesis in the early stages of endometriosis development is needed to determine which molecules could potentially be targeted therapeutically.…”

Section: Pathogenesis and Progression Of Endometriosismentioning

confidence: 95%

Endometriosis: where are we and where are we going?

Greene¹,

Lang²,

Kendziorski³

et al. 2016

Reproduction

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Endometriosis currently affects ∼5.5 million reproductive-aged women in the U.S. with symptoms such as painful periods (dysmenorrhea), chronic pelvic pain, pain with intercourse (dyspareunia), and infertility. It is defined as the presence of endometrial tissue outside the uterine cavity and is found predominately attached to sites within the peritoneal cavity. Diagnosis for endometriosis is solely made through surgery as no consistent biomarkers for disease diagnosis exist. There is no cure for endometriosis and treatments only target symptoms and not the underlying mechanism(s) of disease. The nature of individual predisposing factors or inherent defects in the endometrium, immune system, and/or peritoneal cavity of women with endometriosis remains unclear. The literature over the last 5 years (2010-2015) has advanced our critical knowledge related to hormones, hormone receptors, immune dysregulation, hormonal treatments, and the transformation of endometriosis to ovarian cancer. In this review, we cover the aforementioned topics with the goal of providing the reader an overview and related references for further study to highlight the progress made in endometriosis research, while concluding with critical areas of endometriosis research that are urgently needed.

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MicroRNA expression profile in endometriosis: its relation to angiogenesis and fibrinolytic factors

Cited by 132 publications

References 56 publications

Microarray analysis of microRNA deregulation and angiogenesis-related proteins in endometriosis

Microarray analysis of microRNA deregulation and angiogenesis-related proteins in endometriosis

MicroRNA-17 downregulates expression of the PTEN gene to promote the occurrence and development of adenomyosis

Endometriosis: where are we and where are we going?

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