Exosome-mediated microRNA-138 and vascular endothelial growth factor in endometriosis through inflammation and apoptosis via the nuclear factor-κB signaling pathway

Aifeng Zhang, Guoyun Wang, Lihua Jia, Tao Su, Lili Zhang
International journal of molecular medicine · 2018 · vol. 43(1) , pp. 358–370 · doi:10.3892/ijmm.2018.3980 · PMID:30431056 · W2900136447
article OA: hybrid CC0 ⤵ 22 in-corpus citations
🔓 Open OA copy View on OpenAlex View on PubMed View at publisher

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.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Apoptosis Endometriosis Exosomes Inflammation MicroRNAs NF-kappa B Signal Transduction Vascular Endothelial Growth Factor A Animals Apoptosis Cell Line, Tumor Cell Proliferation Coculture Techniques Disease Models, Animal Endometriosis Endometriosis Endothelial Cells Endothelial Cells Exosomes Female

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (29)

Cited by (22)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:19:25.021412+00:00
License: CC0 · commercial use OK