[Gly14]-Humanin Ameliorates High Glucose-Induced Apoptosis by Inhibiting the Expression of MicroRNA-155 in Endothelial Microparticles.
Shen. Meng-Yuan MY; Wang. Miao M; Liu. Zhihua Z; Wang. Shurong S; Xie. Ying Y
Key Findings
- High glucose raises the number of endothelial microparticles and the harmful miR‑155 they carry, increasing cell death.
- Pretreating cells with HNG cuts down both the microparticle count and miR‑155 levels, reducing apoptosis.
- Adding extra miR‑155 cancels HNG’s protective effect, while blocking miR‑155 boosts it, confirming the pathway.
Practical Outcomes
- Humanin (or its Gly14‑enhanced version) could be explored as a vascular‑protective supplement for people dealing with high blood sugar or diabetes. Until human trials are done, biohackers might consider low‑dose humanin peptides as an experimental addition, watching for any effects on blood‑pressure, circulation, or metabolic markers, but should treat it as a speculative, not proven, intervention.
Summary
A special form of the peptide humanin (called HNG) can protect blood‑vessel cells from dying when they’re exposed to high sugar levels. It does this by stopping tiny particles released by cells (called endothelial microparticles) from carrying a harmful micro‑RNA (miR‑155) that triggers cell death. The work is done in lab dishes, not people, but it hints that humanin‑based supplements might help guard blood vessels in diabetes or high‑sugar situations.
Abstract
Humanin, 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. EMPs 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. We 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. HNG 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.
Study Information
pubmed
2021
2021-05-24T00:00:00.000Z
10.2147/dmso.s306026