MECHANICAL STRESS REDUCES APOPTOSIS‑RELATED SIGNALING IN CULTURED NEURONS

A variety of cell types are sensitive to mechanical stress, eliciting intracellular signaling through cellular mechanotransduction. Recent studies have increasingly highlighted the possibility that neurons in the central nervous system (CNS) possess intrinsic mechanosensitivity. CNS neurons have been reported to express mechanosensitive channels, including TRP and Piezo family members, which can activate MAPK signaling pathways implicated in synaptic plasticity and neuronal survival. In this study, we investigated whether mechanical stress contributes to neuroprotection in CNS neurons by examining its effects on apoptosis‑related signaling in cultured neurons.
Neural progenitor cells were isolated from the mouse cerebellum and maintained in Neurobasal medium supplemented with 1% penicillin–streptomycin and 2% B-27. The cells were subsequently treated with AraC and differentiated into neurons, forming neuronal networks on the culture plate. Mechanical stress was applied to the “shaking” group by oscillating the culture plate at 1 Hz at 37 °C for 30 min per day over five days. In contrast, the “non‑shaking” control group was kept at 37 °C without mechanical stimulation. Following the intervention, mRNA was extracted from the collected cells and subjected to quantitative PCR to assess the expression of apoptosis‑related genes, including caspase‑3.
Five days of shaking significantly reduced caspase‑3 expression in neurons, suggesting that mechanical stress attenuates apoptotic potential.
This finding indicates that neurons can sense mechanical stress and that such stimuli may promote neuronal protection and survival. Further investigations are warranted to elucidate the mechanotransduction pathways responsible for these beneficial effects in neurons.