Significance: In specific tissues, cell death does not represent the end of cell function. The death of the uppermost stratum granulosum keratinocytes (SG1 cells) facilitates their conversion into stratum corneum (SC) corneocytes. Such cells are not removed by efferocytosis as would occur after apoptosis or necrosis; instead, nonviable cell bodies contribute to the protective barrier function of the SC. The present study demonstrates that SG1 cell death is initiated via a single episode of prolonged intracellular Ca ²⁺ elevation, followed by rapid acidification. Such intracellular ionic changes facilitate organellar degradation events specific to SC corneocyte formation. These findings further expand the current knowledge on cell death modes and highlight that nonviable cells contribute to physiological functions in specific contexts.

Ultrabroadband spectroscopy reveals modulation of the water relaxations induced by hydrogen-bond dynamics at short times.