Exosomal lncRNA ENST00000592016 rescues the Weakened Viability of HUVEC Cells Caused by Intermittent Hypoxia.
Wu Z., Lai X., Zhao Y., Hong J., Liu Y., Liang H.
Prospective Study, published in Comb Chem High Throughput Screen (2025) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Prospective Study
- Journal
- Comb Chem High Throughput Screen (2025)
- Country
- United Arab Emirates
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40464189
- DOI
- 10.2174/0113862073355701250512034857
Abstract (original English)
Background Obstructive sleep apnea syndrome [OSAS] is a common sleep breathing disorder accompanied by multiple organ intermittent hypoxemia. Our previous study has suggested that the expression of a lncRNA termed ENST00000592016 [lnc2016 for short] derived from plasma exosomes is remarkably elevated in OSA patients compared to the normal population, and lnc2016 can improve the diagnostic efficiency of OSA. Objective To unmask the role of the lnc2016 in vascular endothelial cells, targeted hypoxia is the goal of the current research. Methods Primary human ADSCs and HUVEC cells were cultured. CCK-8, cytometric assay, transwell, and tubular formation assay were used to determine cell viability, cell apoptosis, cell cycle, cell migration, as well as tubular formation ability. Results we found that adipose-derived stem cells [ADSCs]-derived exosomes contained robust lnc2016. After co-culture with human umbilical vein endothelial cells [HUVECs], exosomal lnc2016 could enhance cell proliferation, DNA synthesis, migration, and tubular formation, whereas suppress cell apoptosis of HUVECs against hypoxic conditions. Conclusion Our data have revealed that ln2016 can promote the cell growth, migration, DNA synthesis, and tubular formation as well as suppress the cell apoptosis of vascular endothelial cells against hypoxia in vitro.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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