Selenium deficiency negatively affects survival and integrity of human hippocampal progenitor cells.

Selenium has been shown to be a key regulatory element in the health, survival and proliferation of neural stem and progenitor cells, with various studies underlining its anti-aging properties. However, most of this knowledge is derived from rodent models, leaving its effects on human hippocampal progenitor cells unclear. In this study, we utilized a human hippocampal progenitor cell (HPC) line to examine the effects of varying concentrations of sodium selenite, an inorganic form of selenium (0 µM, 0.1 µM, 0.23 µM, 0.5 µM, and 1.0 µM), on the proliferation, apoptosis, and progenitor integrity of these cells. To do this, HPCs were exposed to these concentrations for 48 h, followed by immunocytochemistry to quantify, cell number (DAPI-positive cells), proliferation (KI67-positve cells), apoptosis (CC3-positve cells), and progenitor integrity (SOX2- and Nestin-positive cells). While our results indicated no significant effects of selenium concentrations on proliferation or apoptosis, we demonstrated that absence of selenium (0 μM) in the culture media significantly reduced both cell number and percentage of Nestin-positive cells, but only when compared to the condition with the highest selenium concentration (1.0 μM). Our findings underscore the role of selenium in regulating the survival and integrity of human HPCs. Lastly, we emphasize the need for further research to uncover the mechanisms underlying these observed changes.