miRNA-223 expression in patient-derived eutopic and ectopic endometrial stromal cells and its effect on epithelial-to-mesenchymal transition in endometriosis

Yuan, Xueliang; Shi, Tingting; Yongjie, Tian

doi:10.1016/j.clinsp.2022.100112

Cited by 5 publications

(2 citation statements)

References 23 publications

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“…Exosomes derived from macrophages tend to accumulate in inflammatory sites, potentially producing a proinflammatory response [ 105 ]. It has been reported that exosomal miR-223 induced the differentiation of M2 macrophages from monocytes as well as other progenitor cell lineages that eventually mature into granulocytes or megakaryocytes, which are produced by endothelial cells, epithelial cells, and fibroblasts in the inflammatory state [ 106 , 107 ]. Additionally, miR-223 , released from macrophage-derived EVs via the PTEN-PI3K/AKT pathway, promoted a malignant phenotype in epithelial ovarian cancer (EOC) cells [ 108 ].…”

Section: Macrophage-derived Evs In the Pathogenesis Of Emsmentioning

confidence: 99%

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The Extracellular Vesicle–Macrophage Regulatory Axis: A Novel Pathogenesis for Endometriosis

Gao,

Shao

et al. 2023

Biomolecules

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Endometriosis (EMs) is a common disease among women whose pathogenesis is still unclear, although there are various hypotheses. Recent studies have considered macrophages the key part of the immune system in developing EMs, inducing inflammation, the growth and invasion of the ectopic endometrium, and angiogenesis. Extracellular vesicles (EVs) as novel intercellular vesicle traffic, can be secreted by many kinds of cells, including macrophages. By carrying long non-coding RNA (lncRNA), microRNA (miRNA), or other molecules, EVs can regulate the biological functions of macrophages in an autocrine and paracrine manner, including ectopic lesion growth, immune dysfunction, angiogenesis, and can further accelerate the progression of EMs. In this review, the interactions between macrophages and EVs for the pathogenesis of EMs are summarized. Notably, the regulatory pathways and molecular mechanisms of EVs secreted by macrophages during EMs are reviewed.

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Section: Macrophage-derived Evs In the Pathogenesis Of Emsmentioning

confidence: 99%

“…This finding also echoed the results in EMs. Upregulation of miRNA-223 has been observed to attenuate the migratory and invasive capability of ESCs in Ems, while suppressing cell apoptosis [ 107 ]. However, the direct effect of exosomal miR-223 on macrophages in EMs needs further elucidation.…”

Section: Macrophage-derived Evs In the Pathogenesis Of Emsmentioning

confidence: 99%

The Extracellular Vesicle–Macrophage Regulatory Axis: A Novel Pathogenesis for Endometriosis

Gao,

Shao

et al. 2023

Biomolecules

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Interactions between miRNAs and the Wnt/β-catenin signaling pathway in endometriosis

Zhang,

Sun,

et al. 2024

Biomedicine & Pharmacotherapy

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Effects of Recepteur D’origine Nantais/Phosphatidylinositol 3 Kinase Pathway Mediated by Polymer Biodegradable Sustained-Release Materials on Proliferation and Apoptosis of Uterine Fibroids

Wang,

Liu

2023

sci adv mater

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This research was aimed to investigate the effects of biodegradable letrozole (LE) sustained release (SR) polymer material on the biological behavior of uterine fibroids (UFs) and RON/PI3K signaling pathway (SPW). Poloxamer 188 (P188) and poly L lactide acid (PLLA) were selected to prepare the degradable SR electrospinning (ES) materials LE/P188/PlLA-1 (LE concentration: 6.25%), LE/P188/PLLA-2 (LE concentration: 12.25%), and LE/P188/PLLA-3 (LE concentration: 25%) with different concentrations of LE. UF cells were then co-cultured with free LE and degradable SR ES materials. Cell proliferation and apoptosis were detected by MTT and flow cytometry, respectively. The expression changes of apoptosis-related proteins (Bcl-2, Bax, and caspase-3), epithelial-mesenchymal transition (EMT)-related proteins (E-cadherin, N-cadherin, Vimentin), and RON/PI3K SPW-related proteins (RON and PI3K) were detected by western blot. The average diameter of LE/P188/PLLA-1, LE/P188/PLLA-2, and LE/P188/PLLA-3 were (145.6±20.8) nm, (158.1±16.3) nm, and (173.4±20.1) nm, respectively. Moreover, it possessed the obvious characteristics of LE, P188, and PLLA. LE/P188/PLLA-3 had the lowest SR rate of LE but the longest SR duration. Compared with normal cells, the proliferation inhibition rate (PIR) and apoptosis rate (AR) of LE and its degradable SR ES materials were increased (P <0.05). While expressions of Bax, caspase-3, E-cadherin, and PI3K were increased, Bcl-2, N-cadherin, Vimentin, and RON were decreased (P <0.05). In contrast to the free LE, the cell proliferation inhibition rate (PIR) and apoptosis promotion rate (APR) of LE degradable SR ES materials were increased, the levels of Bax, caspase-3, E-cadherin, and PI3K were increased, and the levels of Bcl-2, N-cadherin, Vimentin, and RON were decreased (P <0.05). The results herein were concentration-dependent. The preparation of LE degradable SR ES materials with P188/PLLA can improve the therapeutic effect of LE. LE degradable SR ES materials can effectively inhibit the proliferation of UFs, promote cell apoptosis, inhibit its EMT process and activation of RON/PI3K SPW in a concentration-dependent manner.

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miRNA-223 expression in patient-derived eutopic and ectopic endometrial stromal cells and its effect on epithelial-to-mesenchymal transition in endometriosis

Cited by 5 publications

References 23 publications

The Extracellular Vesicle–Macrophage Regulatory Axis: A Novel Pathogenesis for Endometriosis

The Extracellular Vesicle–Macrophage Regulatory Axis: A Novel Pathogenesis for Endometriosis

Interactions between miRNAs and the Wnt/β-catenin signaling pathway in endometriosis

Effects of Recepteur D’origine Nantais/Phosphatidylinositol 3 Kinase Pathway Mediated by Polymer Biodegradable Sustained-Release Materials on Proliferation and Apoptosis of Uterine Fibroids

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