ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2021
[Gly14]-Humanin Ameliorates High Glucose-Induced Apoptosis by Inhibiting the Expression of MicroRNA-155 in Endothelial Microparticles.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- [Gly14]-Humanin ameliorates high glucose-induced endothelial senescence via SIRT6.Scientific reports · 2024Article
- Mitochondrial-derived peptides in cardiovascular disease: Novel insights and therapeutic opportunities.Journal of advanced research · 2024Review
- MicroRNA Cues from Nature: A Roadmap to Decipher and Combat Challenges in Human Health and Disease?Cells · 2021Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHumanin, a newly emerging endogenously expressed cytoprotective peptide, has been shown to have anti-apoptotic properties effects by protecting neuronal cells injury. Endothelial microparticles (EMPs) are considered as vital mediators in intercellular communication. EMPs may regulate various physiological and pathological processes by transferring mRNAs and microRNAs (miRNAs) to recipient cells.
methodsEMPs were isolated from human umbilical vein endothelial cells (HUVECs) by ultracentrifugation. EMPs were characterized by transmission electron microscopy and nanoparticle tracking analyses. Observation of EMPs uptake into HUVECs and the number of EMPs were realized by confocal microscopy. The expression of miR-155 was examined using real-time PCR. Cell apoptosis was examined by flow cytometry assay.
resultsWe found that high glucose (HG) increased the number of EMPs and upregulated the expression of miR-155 contained within EMPs, which was mitigated by HNG pretreatment. miR-155 overexpression in EMPs reversed the effects of HNG pretreatment and increased apoptosis of target cells. Effects of HNG pretreatment on HG-treated endothelial cells (ECs) were mitigated after miR-155 mimic transfection into HUVECs while were augmented after miR-155 inhibitor transfection into HUVECs.
conclusionHNG inhibited HG-induced apoptosis of ECs and the effect of HNG may be mediated by inhibiting the transfer of EMPs miR-155 from HG-induced HUVECs to normal cells. This study provides a new direction for biological products related to humanin to treat vascular complications associated with all forms of diabetes mellitus.
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