Endometrial-Peritoneal Interactions during Endometriotic Lesion Establishment

Hull, M. Louise; Rangel‐Escareño, Claudia; Godsland, Jane M.; Doig, John R.; Johnson, Claire M.; Phillips, Stephen C.; Smith, Stephen K.; Tavaré, Simon; Print, Cristin G.; Charnock-Jones, D. Stephen

doi:10.2353/ajpath.2008.071128

Cited by 142 publications

(115 citation statements)

References 72 publications

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“…Interestingly, a recent report also indicates up-regulation of collagen, lumican, and caldesmon at the transcript level in ECE (40). Investigations by others also suggest an increase in total collagen (40,41) as well as the increased presence of collagen VI in endometriotic cysts (42). Caldesmon, an actin-and calmodulin-binding protein, is associated with podosomes.…”

Section: Figurementioning

confidence: 84%

“Spot”-ting differences between the ectopic and eutopic endometrium of endometriosis patients

Chehna-Patel

Sachdeva

Gajbhiye

et al. 2010

Fertility and Sterility

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Section: Figurementioning

confidence: 84%

“Spot”-ting differences between the ectopic and eutopic endometrium of endometriosis patients

Chehna-Patel

Sachdeva

Gajbhiye

et al. 2010

Fertility and Sterility

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“…Some authors have previously stated that human endometrial tissues transplanted in mice derive their blood supply from the surrounding vascular network, with the original human vessel simultaneously disappearing as the mouse vessels invade the stroma (Grü mmer 2001, Bruner-Tran et al 2002, Hull et al 2003, Eggermont et al 2005. However, recent studies have revealed the presence of mouse, human, and functional chimeric human-mouse vessels throughout such grafts (Masuda et al 2007, Similarly, host-derived cell types, such as macrophages and myofibroblasts, have been shown to coexist with macrophages from human endometrium embedded in the stroma of immunocompromised mouse xenografts (Hull et al 2008, Guo et al 2011. Such studies reveal an interaction between host and graft at different levels, by which a combined structure capable of responding to different stimuli is created.…”

Section: Discussionmentioning

confidence: 99%

“…Angiogenesis involves complex molecular interactions between endometrial tissue, peritoneal tissue, infiltrating leucocytes, and fibroblasts (Hull et al 2008). In addition, the origin of neovasculature in xenografts remains unclear, which further complicates the analysis of these interactions.…”

Section: Discussionmentioning

confidence: 99%

The effects of ergot and non-ergot-derived dopamine agonists in an experimental mouse model of endometriosis

Delgado-Rosas¹,

Gómez²,

Ferrero³

et al. 2011

Reproduction

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Implantation of a retrogradely shed endometrium during menstruation requires an adequate blood supply, which allows the growth of endometriotic lesions. This suggests that the development of endometriosis can be impaired by inhibiting angiogenesis. The growth of endometriotic foci is impaired by commercial oncological antiangiogenic drugs used to block vascular endothelial growth factor (VEGF) signaling. The dopamine agonist cabergoline (Cb2) inhibits the growth of established endometriosis lesions by exerting antiangiogenic effects through VEGFR2 inactivation. However, the use of ergot-derived Cb2 is associated with an increased incidence of cardiac valve regurgitation. To evaluate the potential usage of non-ergot-derived dopamine agonists for the treatment of human endometriosis, we compared the efficacy of quinagolide with that of Cb2 in preventing angiogenesis and vascularization in a heterologous mouse model of endometriosis. Nude mice whose peritoneum had been implanted with eutopic human endometrial fragments were treated with vehicle, 50 mg/kg per day oral Cb2, or 50 or 200 mg/kg per day quinagolide during a 14-day period. At the end of the treatment period, the implants were excised in order to assess lesion size, cell proliferation, degree of vascularization, and angiogenic gene expression. Neoangiogenesis was inhibited and the size of active endometriotic lesions, cellular proliferation index, and angiogenic gene expression were significantly reduced by both dopamine agonists when compared with the placebo. Given that Cb2 and quinagolide were equally effective in inhibiting angiogenesis and reducing lesion size, these experiments provide the rationale for pilot studies to explore the use of non-ergot-derived dopamine agonists for the treatment of endometriosis in humans.

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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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Endometrial-Peritoneal Interactions during Endometriotic Lesion Establishment

Cited by 142 publications

References 72 publications

“Spot”-ting differences between the ectopic and eutopic endometrium of endometriosis patients

“Spot”-ting differences between the ectopic and eutopic endometrium of endometriosis patients

The effects of ergot and non-ergot-derived dopamine agonists in an experimental mouse model of endometriosis

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

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