ArticleAmerican journal of translational research2023
Mesenchymal stem cell-derived exosomes ameliorate TGF-β1-induced endometrial fibrosis by altering their miRNA profile.
Article in American journal of translational research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 3 citations in OpenAlex.
- Evolution of biotechnological advances and regenerative therapies for endometrial disorders: a systematic review.Human reproduction update · 2024Pooled it
- Endometrial Repair and Regenerative Medicine: From Broad-Spectrum Regeneration to Precision Intervention.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Review
- Integrative bioengineering strategies for endometrial regeneration: From biomaterials and stem cells to organoids and organ-on-a-chip technologies.Theranostics · 2026Review
- Extracellular vesicles secreted by equine adipose mesenchymal stem cells preconditioned with transforming growth factor β-1 are enriched in anti-fibrotic miRNAs and inhibit the expression of fibrotic genes in an in vitro system of endometrial stromal cells fibrosis.The veterinary quarterly · 2024Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveMesenchymal stem cell (MSC)-derived exosomes (MSC-exo) can treat reproductive disorders. However, the action of microRNAs (miRNAs) in this mechanism has yet to be systematically investigated. This study aimed to explore the effect of MSC-exo on TGF-β1-induced endometrial fibrosis in intrauterine adhesions and elucidate the regulatory mechanisms involved in key genes by comparing miRNA expression profiles.
methodsMSC-exo were isolated and identified based on particle size and protein marker detection. Cell counting kit-8, flow cytometry, and western blotting were used to determine the effects of MSC-exo on cell function and fibrosis in human endometrial epithelial cells (hEECs). Subsequently, we sequenced and annotated the small RNA in MSC-exo and TGF-β1-induced MSC-exo to screen for differentially expressed (DE) miRNAs. After the prediction and functional enrichment of target genes of DE miRNAs, key genes were selected for functional experiments.
resultsTGF-β1 inhibited the proliferation of hEECs and promoted apoptosis and fibrosis. However, these effects were significantly reversed by the addition of MSC and MSC-exo. Fifteen DE miRNAs were identified by comparing the miRNA profiles of MSC-exo and TGF-β1-induced MSC-exo. Among these, miR-145-5p was found to be significantly upregulated in TGF-β1-induced MSC-exo. Furthermore, the addition of miR-145-5p mimic was found to reverse fibrosis in hEECs while promoting the expression of key autophagy protein P62.
conclusionMSC-exo ameliorated TGF-β1-induced endometrial fibrosis. RNA sequencing, bioinformatic analysis, and functional experiments revealed that miR-145-5p may exert its action through the P62-dependent autophagy pathway.
Indexed as
Identifiers
37303669PMC10250987W4380290420What OpenQuestion holds
Registered trials
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.