Aromatase, microRNA, and inflammation: a complex relationship

Bulun, Serdar E.; Nezhat, Camran

doi:10.1016/j.fertnstert.2016.06.045

Cited by 7 publications

(6 citation statements)

References 5 publications

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“…High aromatase expression has been also observed in the eutopic endometrium as well as in endometriosis implants . This enzymatic imbalance is thought to raise oestrogen activity into the endometriotic lesion, maintaining the loop between local hyperoestrogenic state, inflammation and proliferation and survival of endometriotic implants . Endometriosis current treatment is thus mainly based on suppression of oestrogen production.…”

Section: Introductionmentioning

confidence: 99%

Effect of local aromatase inhibition in endometriosis using a new chick embryo chorioallantoic membrane model

Pluchino

Poppi

Yart

et al. 2019

J Cellular Molecular Medi

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Endometriosis is an oestrogen‐dependent, inflammation‐driven gynaecologic disorder causing severe disability. Endometriosis implants are characterized by unbalanced local oestrogen metabolism leading to hyperoestrogenism and aromatase up‐regulation is one of main mechanism involved. Aromatase inhibitors such as letrozole or anastrozole use in young women are associated with severely side effects limiting their long‐term clinical use. An endometriosis‐targeted inhibition of local aromatase could be a viable alternative, although the role of the local inhibition of this enzyme is still unclear. Using a new chick embryo allantoic membrane (CAM) model incorporating xenografted human endometriosis cyst, we showed that topical treatment with anastrozole reduced lesion size, although oestrogens produced by CAM female embryo blunted this effect. Xenografted human endometriosis CAM is a new efficient model for the screening of new drugs targeting endometriosis tissue.

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Section: Introductionmentioning

confidence: 99%

Effect of local aromatase inhibition in endometriosis using a new chick embryo chorioallantoic membrane model

Pluchino

Poppi

Yart

et al. 2019

J Cellular Molecular Medi

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“…Another study also demonstrated that the elevated expression of HMGB1 is closely associated with the occurrence of sepsis ( 5 ). miRs are highly conserved, endogenous, non-coding small RNAs, which can regulate the expression of target genes by complete or incomplete complementary pairing with the 3′-untranslated region (3′-UTR) of the mRNA, serving an important role in immune cell activation, inflammatory cytokine release and the immune response ( 6 , 7 ). Previous research has revealed that miR-25 was involved in the occurrence and progression of sepsis and has potential as a diagnostic marker of sepsis ( 8 , 9 ).…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effects of miR‑25 targeting HMGB1 on macrophage secretion of inflammatory cytokines in sepsis

2018

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High mobility group box 1 (HMGB1) can promote the migration of macrophages and the release of inflammatory cytokines, functions associated with the occurrence of sepsis. The role of microRNA (miR)-25 in the targeted regulation of HMGB1 expression and the release of macrophage inflammatory cytokines remains uncharacterized. The present study investigated the association between miR-25, HMGB1 and sepsis by analyzing the expression of miR-25 and HMGB1 in patients with sepsis. The present study also investigated whether miR-25 serves a role in targeting the regulation of HMGB1 expression and macrophage inflammatory factor release. Patients with sepsis were selected from the Intensive Care Unit, and serum levels of HMGB1. The expression of miR-25 and HMGB1 in serum and peripheral blood mononuclear cells (PBMCs) was compared. Macrophages were cultured in vitro and divided into 5 groups following treatment with lipopolysaccharide (LPS). The expression levels of miR-25, HMGB1, phosphorylated (p-)p65, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and HMGB-1 were compared, and the migration ability of cells was investigated by Transwell assays. Compared with the healthy controls, patients with sepsis exhibited elevated expression of HMGB1 and decreased expression of miR-25 in serum and PBMCs. Following treatment with LPS, the expression of HMGB1 and p-p65 was elevated, and the expression of miR-25 was decreased in macrophages compared with untreated cells. Following transfection with miR-25 mimics and/or short interfering RNA-HMGB1, the expression of HMGB1 in macrophages decreased significantly, the expression of p-p65, HMGB-1, TNF-α and IL-6 in the culture solution were also decreased, and the migration ability of macrophages was attenuated. The present study suggests that miR-25 attenuated the induction of HMGB1 by LPS, decreased the activity of nuclear factor-κB and the transcriptional activation of TNF-α and IL-6, and suppressed the migration of macrophages. Inhibiting expression of miR-25 may serve a role in upregulating HMGB1 expression, promoting the secretion of inflammatory cytokines and resulting in sepsis.

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“…Expression of aromatase by endometriotic stromal cells accounts for the local increase in E 2 production in ectopic implants . Moreover, the peritoneal fluid of women with endometriosis contains significantly higher levels of pro‐angiogenic and/or pro‐inflammatory cytokines VEGF, IL‐8, and MCP‐1 .…”

Section: Discussionmentioning

confidence: 99%

The extracellular signal‐regulated kinase 1/2 triggers angiogenesis in human ectopic endometrial implants by inducing angioblast differentiation and proliferation

Arlıer

Murk

Guzeloglu‐Kayisli

et al. 2017

American J Rep Immunol

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Aromatase, microRNA, and inflammation: a complex relationship

Cited by 7 publications

References 5 publications

Effect of local aromatase inhibition in endometriosis using a new chick embryo chorioallantoic membrane model

Effect of local aromatase inhibition in endometriosis using a new chick embryo chorioallantoic membrane model

Inhibitory effects of miR‑25 targeting HMGB1 on macrophage secretion of inflammatory cytokines in sepsis

The extracellular signal‐regulated kinase 1/2 triggers angiogenesis in human ectopic endometrial implants by inducing angioblast differentiation and proliferation

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