ArticleJournal of cellular and molecular medicine2021
microRNA-106b derived from endothelial cell-secreted extracellular vesicles prevents skin wound healing by inhibiting JMJD3 and RIPK3.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Extracellular vesicle microRNA cargoes: candidates for diagnosis and targeted therapy of cutaneous wound healing.Annals of medicine · 2025Review
- Deciphering the Molecular Dialogue: Mitochondria, Epigenetics, and Extracellular Vesicles in Placental Function and Pregnancy Complications.Comprehensive Physiology · 2025Review
- GelMA hydrogel-loaded extracellular vesicles derived from keratinocytes promote skin microvasculature regeneration and wound healing in diabetic mice through activation of the PDGF-induced PI3K/AKT pathway.Cell biology and toxicology · 2025Article
- Exosome Source Matters: A Comprehensive Review from the Perspective of Diverse Cellular Origins.Pharmaceutics · 2025Review
- New insights into microRNA in dermatological diseases.Frontiers in medicine · 2025Review
- Article
- AGEs impair osteogenesis in orthodontic force-induced periodontal ligament stem cells through the KDM6B/Wnt self-reinforcing loop.Stem cell research & therapy · 2024Article
- Role of exosome-derived miRNAs in diabetic wound angiogenesis.Molecular and cellular biochemistry · 2024Review
- Emerging role of Jumonji domain-containing protein D3 in inflammatory diseases.Journal of pharmaceutical analysis · 2024Review
- Extracellular Vesicles: Emergent and Multiple Sources in Wound Healing Treatment.International journal of molecular sciences · 2023Review
- JMJD3 regulates diabetic wound repair in a STINGy fashion.Cellular & molecular immunology · 2023Article
- Macrophage-specific inhibition of the histone demethylase JMJD3 decreases STING and pathologic inflammation in diabetic wound repair.Cellular & molecular immunology · 2022Article
- Beyond the Code: Noncoding RNAs in Skin Wound Healing.Cold Spring Harbor perspectives in biology · 2022Article
- Native and engineered extracellular vesicles for wound healing.Frontiers in bioengineering and biotechnology · 2022Review
- Landscape of the epigenetic regulation in wound healing.Frontiers in physiology · 2022Review
- microRNA-106b derived from endothelial cell-secreted extracellular vesicles prevents skin wound healing by inhibiting JMJD3 and RIPK3.Journal of cellular and molecular medicine · 2021Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intriguingly, microRNAs (miRs) transferred as cargo in extracellular vesicles (EVs) can modulate wound healing through their regulation of fibroblast functions. In this study, we investigated the effects of miR-106b transfer via EVs derived from human umbilical vein endothelial cells (HUVECs) on skin wound healing. Dual-luciferase reporter gene assay identified that miR-106b could target and inhibit JMJD3. RT-qPCR analysis showed EVs isolated from HUVECs had enriched expression of miR-106b. LL29 fibroblast cells and HaCaT keratinocytes were co-cultured with HUVEC-derived EVs, in which miR-106b had been up-regulated or down-regulated by its mimic or inhibitor. The co-culture with HUVEC-derived EVs increased miR-106b expression, and reduced the viability and adhesion of LL29 and HaCaT cells, whereas the inhibition of miR-106b in HUVEC-derived EVs enhanced the viability and adhesion of LL29 and HaCaT cells through up-regulation of JMJD3. Next, we showed that JMJD3 overexpression enhanced LL29 and HaCaT cell viability and adhesion through elevating RIPK3, which induced the phosphorylation of AKT during the wound-healing process. We next developed a mouse skin wound model to investigate the actions of miR-106b in vivo after 14 days. The delivery of miR-106b via HUVEC-derived EVs delayed wound healing through suppression of collagen I content and angiogenesis, but had no effects on pro-inflammatory cytokines. In conclusion, miR-106b from HUVEC-derived EVs inhibits JMJD3 and RIPK3, leading to the inhibition of skin wound healing, thus constituting a new therapeutic target.
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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.