ArticleInternational journal of molecular medicine2019
Exosome-mediated microRNA-138 and vascular endothelial growth factor in endometriosis through inflammation and apoptosis via the nuclear factor-κB signaling pathway.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- A bibliometric analysis of exosomes in aging from 2007 to 2023.Frontiers in medicine · 2024Pooled it
- Therapeutic Potential of Linalool in Endometriosis: Modulation of Oxidative Stress, Inflammation, and Apoptosis in a Rat Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Evaluating the Effect of Exosome-Encapsulated miR-4289 on Menstrual Blood-Derived Mesenchymal Stem Cells from Endometriosis Patients.Biochemical genetics · 2026Article
- Role of Fisetin in the Mammalian Reproductive System.Veterinary sciences · 2026Review
- Endometriosis-derived exosomal MicroRNA-125b-5p downregulates phosphatidylinositol 3-Kinase/Protein Kinase B signaling pathways via vascular endothelial growth factor to decelerate endometriosis progression.Molecular biology reports · 2026Article
- Endometriosis as a Systemic and Complex Disease: Toward Phenotype-Based Classification and Personalized Therapy.International journal of molecular sciences · 2026Review
- Dysregulation of Key Biological Processes in Endometriosis Pathophysiology.Current molecular medicine · 2026Review
- Endometriosis-derived exosomes encapsulated miR-196a-5p mediate macrophage polarization through regulation of the Hippo pathway.Journal of cell communication and signaling · 2025Article
- Review
- The bovine oviductal environment and composition are negatively affected by elevated body energy reserves.PloS one · 2025Article
- GEVResearch (Washington, D.C.) · 2025Article
- Novel Insights Into DLAT's Role in Alzheimer's Disease-Related Copper Toxicity Through Microglial Exosome Dynamics.CNS neuroscience & therapeutics · 2024Article
- Extracellular Vesicles: the Next Frontier in Pregnancy Research.Reproductive sciences (Thousand Oaks, Calif.) · 2024Review
- Regulatory RNAs in immunosenescence.Immunity, inflammation and disease · 2024Review
- Exosomes of endothelial progenitor cells repair injured vascular endothelial cells through the Bcl2/Bax/Caspase-3 pathway.Scientific reports · 2024Article
- Regulated Cell Death in Endometriosis.Biomolecules · 2024Review
- Extracellular vesicles in endometriosis: role and potential.Frontiers in endocrinology · 2024Review
- The Pathological Role of miRNAs in Endometriosis.Biomedicines · 2023Review
- MicroRNAs in Endometriosis: Insights into Inflammation and Progesterone Resistance.International journal of molecular sciences · 2023Review
- Exosomal microRNAs and long noncoding RNAs: as novel biomarkers for endometriosis.Cell and tissue research · 2023Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometriosis (Ems) is a condition that refers to the ectopic implantation and growth of endometrial tissue outside the uterine cavity. The aim of the present study was to investigate the role of microRNA‑138 (miR‑138) in Ems and the possible underlying mechanism. Flow cytometry was measured CD11b level, cell proliferation was measured using MTT assay and lactate dehydrogenase (LDH) assays was analyzed using LDH activity kits. Cell apoptosis was measured using Annexin V‑FITC/PI double staining apoptosis detection kit and DAPI assays. ELISA assay and western blot analysis were used to measure protein expression determination. It was first observed that miR‑138 expression was markedly downregulated and the CD11b level was reduced in Ems mice compared with the control group. Subsequently, miR‑138 expression was downregulated in the uterine endothelial cells co‑cultured with THP‑1 cells, which resulted in decreased apoptosis and increased inflammation in the uterine endothelial cells. By contrast, upregulation of miR‑138 by mimic transfection increased the proliferation and reduced inflammation in uterine endothelial cells. In addition, in the co‑culture of uterine endothelial and THP‑1 cells, downregulation of miR‑138 induced the expression of nuclear factor (NF)‑κB and vascular endothelial growth factor (VEGF) proteins in THP‑1 cells. Furthermore, treatment with an NF‑κB inhibitor and downregulation of miR‑138 in the co‑culture of uterine endothelial and THP‑1 cells reduced inflammation. VEGF inhibitor treatment and downregulation of miR‑138 in this cell co‑culture promoted the proliferation of uterine endothelial cells. These results suggested that uterine endothelial cells promoted miR‑138 to induce exosome‑mediated inflammation and apoptosis in Ems through the VEGF/NF‑κB signaling pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.