microRNAs and angiogenesis in endometriosis

Marí-Alexandre, Josep; García-Oms, Javier; Barceló-Molina, Moisés; Gilabert-Aguilar, Juan; Estellés, Amparo; Braza-Boïls, Aitana; Gilabert-Estellés, Juan

doi:10.1016/s0049-3848(15)50439-8

Cited by 37 publications

(31 citation statements)

References 34 publications

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“…The role of TSP1‐CD47 signaling in inhibiting angiogenesis is clear and has been investigated in various physiological and pathological situations 17,27 . Many studies have reported that angiogenesis is a main feature of endometriosis 31,32 . In our study, we also demonstrated that angiogenesis in ectopic endometrium was higher than in eutopic endometrium.…”

Section: Discussionsupporting

confidence: 70%

TSP1‐CD47‐SIRPα signaling facilitates the development of endometriosis by mediating the survival of ectopic endometrium

Liu

Wei

et al. 2020

American J Rep Immunol

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Problem:To explore whether the thrombospondin-1(TSP1)-CD47-signal regulatory protein alpha (SIRPα) signaling pathway has impacts on the development of endometriosis. Method of study: Endometrial stromal cells (ESCs) originated from ectopic and eutopic endometrial tissues with or without endometriosis. Monocytes (Macrophages) were isolated from peripheral blood and peritoneal fluids with or without endometriosis. The expression levels of molecules were investigated by flow cytometry (FCM), immunohistochemistry (IHC), and RT-qPCR. The concentration of TSP1 was assessed via ELISA. The capacities of angiogenesis and phagocytosis were measured via tube formation assay and phagocytic assay, respectively.

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Section: Discussionsupporting

confidence: 70%

TSP1‐CD47‐SIRPα signaling facilitates the development of endometriosis by mediating the survival of ectopic endometrium

Liu

Wei

et al. 2020

American J Rep Immunol

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“…The majority of these miRNAs are located in the genomically unstable sites, lending to their targeting of oncogenes, tumor suppressor genes, angiogenesis, and genes associated with inflammation or immune function [62], [76]. Functional pathway analyses of miRNA targets showed alterations in genes such as aromatase ( CYP-19 ) and COX-2 as well as those involved in apoptosis and cell-signaling to be differentially expressed in endometriosis [60], [61], [77], [78], [79]. For example, the downregulation of migration inhibitory factor (MIF) in ectopic endometriotic lesions compared to eutopic endometrium has been attributed to the upregulation of miR-451 [80].…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have speculated that endometriosis is an epigenetic disease [57], [58], [59]. MiRNAs play a major role in the development of endometriotic lesions by contributing to mechanisms involving hypoxic injury, inflammation, tissue repair, cell proliferation, extracellular matrix remodeling, and angiogenesis [60], [61]. In endometriosis, miRNA profiling studies have compared ectopic versus eutopic endometrial tissues [60], [62], [63], often concluding that many miRNAs are differentially expressed between the two groups and target genes closely associated with endometriosis.…”

Section: Introductionmentioning

confidence: 99%

Redox regulation of microRNAs in endometriosis-associated pain

2017

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Endometriosis is a chronic, painful condition with unknown etiology. A differential expression of microRNAs in the endometriotic tissues from women with endometriosis with pain compared to those without suggested a plausible role for miRNA or epigenetic mechanisms in the etiology of endometriotic pain. The peritoneal milieu is involved in maintenance of endometriotic lesion and nociception. We recently showed the mechanistic role for oxidized-lipoproteins (ox-LDLs) present in peritoneal fluid (PF) in endometriosis and pain. We explored the possibility of ox-LDLs modulating the expression of miRNAs in a manner similar to PF from women with endometriosis. Expression levels of miRNAs and their predicted nociceptive and inflammatory targets were determined in PF and ox-LDL treated human endometrial cell-lines. Samples from IRB-approved and consented patients with and without endometriosis or pain were used. These were compared to endometrial cell-lines treated with various forms of oxidized-lipoproteins. RNA (including miRNAs) were isolated from treated endometrial cells and expression levels were determined using commercial miRNome arrays. Cell lysates were used in immunoblotting for inflammatory proteins using a protein array. Twenty miRNAs including isoforms of miR-29, miR-181 and let-7 were mutually differentially expressed in cells treated with PF from endometriosis patients with pain and those treated with ox-LDL components. The ox-LDLs and endo-PF treatment also produced significant overexpression of microRNA predicted target genes nerve growth factor, interleukin-6 and prostaglandin E synthase and overexpression of their downstream protein targets Mip1α and MCP1. This study showed similarities between miRNA regulation in PF from endometriotic women and ox-LDLs present in abundance in the PF of these women. Key miRNAs responsible for targeting nociceptive and inflammatory molecules were downregulated in the presence of ox-LDLs and endo-PF, thus playing a role in the etiology of endometriotic pain. These redox-sensitive miRNAs can be of potential use as targets in the treatment of endometriosis-associated pain.

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“…The expression of microRNAs is precisely controlled to achieve optimum cell function and differentiation . MicroRNAs have important target genes whose expression in turn affects many physiological and pathological conditions such as endometriosis …”

Section: Introductionmentioning

confidence: 99%