Authors: K. Orzeł-Gajowik et al.

Journal: Antioxidants & Redox Signaling (2025)

Research Areas: Cell research

Cell Lines: RBE4 (rat brain endothelial cell line)

Summary: This paper investigates how high levels of ammonia affect brain endothelial cells and whether these effects contribute to cerebrovascular dysfunction. The authors show that exposing a rat brain microvascular endothelial cell line (RBE4) to 5 mM ammonia for 24 h triggers features of cellular senescence (increased β-galactosidase activity, elevated p16 and p21 expression, changes in secretory phenotype), and they identify miR-183-5p as a likely mediator: overexpression of miR-183-5p mimics the senescent phenotype, while its inhibition partially rescues it. In vivo, rats subjected to hyperammonemia exhibited reduced cerebrovascular density, reminiscent of age-related vascular decline, supporting the idea that ammonia-induced endothelial senescence could underlie vascular impairments in neurological disorders. The study proposes miR-183-5p as a potential therapeutic target to mitigate ammonia-induced vascular aging. The authors used quantitative live-cell imaging with HoloMonitor® M4 to monitor cell behavior under ammonia exposure including cell proliferation, cell motility.

Keywords: HoloMonitor M4, cell proliferation, cell motility, hyperammonemia, brain endothelial cells, cellular senescence, miR-183-5p, senescence-associated β-galactosidase, p16, p21, cerebrovascular density, RBE4, blood-brain barrier, endothelial dysfunction