Klebsiella pneumoniae-derived extracellular vesicles impair endothelial function by inhibiting SIRT1
Quick Facts
- Publication title: Klebsiella pneumoniae-derived extracellular vesicles impair endothelial function by inhibiting SIRT1
- Journal: Cell Commun Signal
- Year: 2025
- DOI: 10.1186/s12964-024-02002-0
- PMID/PMCID: 39800699; PMC11726972
Research overview
pn) in hypertension development has been emphasized, although the specific mechanisms have not been well understood. Bacterial extracellular vesicles (BEVs) released by Gram-negative bacteria modulate host cell functions by delivering bacterial components to host cells.
Key findings
pn significantly impaired acetylcholine-induced endothelium-dependent relaxation and increased superoxide anion production in endothelial cells in vivo.
pn EVs caused significant endothelial dysfunction, endothelial provocation, and increased blood pressure.
pn EVs reduced the levels of SIRT1 and p-eNOS and increased the levels of NOX2, COX-2, ET-1, and p53 in endothelial cells.
pn EVs on endothelial cells.
Study design
pn EVs were purified from the bacterial suspension using ultracentrifugation and characterized by transmission electron microscopy nanoparticle tracking analysis, and EV marker expression.
Superoxide anion production was measured by confocal microscopy and HUVEC senescence was assessed by SA-β-gal activity.
SIRT1 overexpression or activator was utilized to investigate the underlying mechanisms.
Echo Biotech Role
Echo Biotech contributed EV isolation and purification; the study also used or cited Exosupur®.
Related platforms: Exoomics®, Research Reagents & Tools
Related services and capabilities: EV Isolation & Purification, Research Reagent / Product Supply
Related products or reagents: Exosupur® EV Isolation/Purification Kit
References
Original publication: Klebsiella pneumoniae-derived extracellular vesicles impair endothelial function by inhibiting SIRT1 Cell communication and signaling. 2025. DOI: 10.1186/s12964-024-02002-0. PMID/PMCID: 39800699; PMC11726972.