Differentially expressed genes in eutopic and ectopic endometrium of women with endometriosis

Meola, Juliana; Silva, Júlio César Rosa e; Dentillo, Daniel Blasioli; Silva, Wilson A.; Veiga‐Castelli, Luciana C.; Bernardes, Luciano Ângelo de Souza; Ferriani, Rui Alberto; Paz, Cláudia Cristina Paro de; Giuliatti, Silvana; Martelli, Lúcia Regina

doi:10.1016/j.fertnstert.2008.12.058

Cited by 101 publications

(95 citation statements)

References 63 publications

(62 reference statements)

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“…Studies on the differences in gene expression between the ectopic and eutopic endometrium (17)(18)(19)(20)(21)(22) have found that many genes related to cell adhesion, cell migration, cell proliferation, immune regulation and inflammation are differentially expressed in ectopic vs. eutopic endometrial tissue. In the study by Ohlsson Teague et al (12), it was suggested that c-Jun mRNA expression was significantly increased in endometriosis.…”

Section: Discussionmentioning

confidence: 99%

miR-29c is downregulated in the ectopic endometrium and exerts its effects on endometrial cell proliferation, apoptosis and invasion by targeting c-Jun

Long

Wan

et al. 2015

International Journal of Molecular Medicine

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Abstract. Endometriosis is a prevalent and complex gynecological disease which affects 10% of women of reproductive age. Certain studies have suggested that a substantial number of microRNAs (miRNAs or miRs) are aberrantly or differentially expressed in the ectopic endometrium. To date, to the best of our knowlewdge, there is no report available on the role of miR-29 in the endometrium. In this study, we investigated the expression of the miR-29 family in the endometrium samples from women without endometriosis, as well as in paired ectopic and eutopic endometrium samples by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results revealed that miR-29c was differentially expressed in the paired eutopic and ectopic endometrium samples. In addition, c-Jun was differentially expressed in the ectopic and eutopic endometrial tissues as determined by western blot analysis. Furthermore, the role of miR-29c in endometrial cell proliferation, invasion and apoptosis was examined in vitro. The results revealed that miR-29c exerted its effects on endometrial cells by suppressing cell proliferation and invasion, as well as promoting cell apoptosis. Furthermore, it was found that c-Jun was a novel target of miR-29c, and c-Jun reversed the effects of miR-29c on the proliferation, invasion and apoptosis of endometrial cells. To the best of our knowledge, this study is the first to identify miR-29c as a suppressor of endometriosis. Taken together, our results suggest that miR-29c exerts its effects on endometrial cell proliferation, apoptosis and invasion by inhibiting the expression of c-Jun. Our data may provide a novel potential therapeutic target for the treatment of endometriosis.

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Section: Discussionmentioning

confidence: 99%

miR-29c is downregulated in the ectopic endometrium and exerts its effects on endometrial cell proliferation, apoptosis and invasion by targeting c-Jun

Long

Wan

et al. 2015

International Journal of Molecular Medicine

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“…This disorder is characterised by extrauterine proliferation of endometrial tissue, and though the causes remain unclear numerous inflammatory mediators and pathways show altered expression patterns. Proteomics studies reveal ANXA1 overexpression in glandular epithelia of eutopic endometrium from endometriosis patients versus healthy controls (Li et al 2008), and further in ectopic versus eutopic endometriosis samples (Meola et al 2010). Full-length ANXA1 protein was also detected in peritoneal fluid samples from endometriosis patients, while the receptor FPR2 was also up-regulated in ectopic endometriosis samples (Motohashi et al 2005).…”

Section: Menstrual Functionmentioning

confidence: 99%

Molecular regulators of resolution of inflammation: potential therapeutic targets in the reproductive system

Hutchinson

Rajagopal²,

Sales³

et al. 2011

Reproduction

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Inflammatory processes are central to reproductive events including ovulation, menstruation, implantation and labour, while inflammatory dysregulation is a feature of numerous reproductive pathologies. In recent years, there has been much research into the endogenous mechanisms by which inflammatory reactions are terminated and tissue homoeostasis is restored, a process termed resolution. The identification and characterisation of naturally occurring pro-resolution mediators including lipoxins and annexin A1 has prompted a shift in the field of anti-inflammation whereby resolution is now observed as an active process, triggered as part of a normal inflammatory response. This review will address the process of resolution, discuss available evidence for expression of pro-resolution factors in the reproductive tract and explore possible roles for resolution in physiological reproductive processes and associated pathologies. Reproduction (2011) 142 15-28

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“…In another study, using the same samples, the authors observed a differential expression of the genes MXRA7 and UBA52, located respectively in 17q25 and 19p13, suggesting that these alterations could lead to the development, establishment, and maintenance of the ovarian endometriomas [41].…”

Section: Discussionmentioning

confidence: 88%

Copy number variation analysis reveals additional variants contributing to endometriosis development

Mafra

Mazzotti

Pellegrino

et al. 2016

J Assist Reprod Genet

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Purpose Endometriosis is a gynecological disease influenced by multiple genetic and environmental factors. The aim of the current study was to use SNP-array technology to identify genomic aberrations that may possibly contribute to the development of endometriosis. Methods We performed an SNP-array genotyping of pooled DNA samples from both patients (n = 100) and controls (n = 50). Copy number variation (CNV) calling and association analyses were performed using PennCNV software. MLPA and TaqMan Copy-Number assays were used for validation of CNVs discovered. Results We detected 49 CNV loci that were present in patients with endometriosis and absent in the control group. After validation procedures, we confirmed six CNV loci in the subtelomeric regions, including 1p36. 33, 16p13.3, 19p13.3, and 20p13, representing gains, while 17q25.3 and 20q13.33 showed losses. Among the intrachromosomal regions, our results revealed duplication at 19q13.1 within the FCGBP gene (p = 0.007). Conclusions We identified CNVs previously associated with endometriosis, together with six suggestive novel loci possibly involved in this disease. The intergenic locus on chromosome 19q13.1 shows strong association with endometriosis and is under further functional investigation.

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Differentially expressed genes in eutopic and ectopic endometrium of women with endometriosis

Cited by 101 publications

References 63 publications

miR-29c is downregulated in the ectopic endometrium and exerts its effects on endometrial cell proliferation, apoptosis and invasion by targeting c-Jun

miR-29c is downregulated in the ectopic endometrium and exerts its effects on endometrial cell proliferation, apoptosis and invasion by targeting c-Jun

Molecular regulators of resolution of inflammation: potential therapeutic targets in the reproductive system

Copy number variation analysis reveals additional variants contributing to endometriosis development

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