Open AccessA unique mode of keratinocyte death requires intracellular acidification
Author(s) -
Toshimitsu Matsui,
Nanako Kadono-Maekubo,
Yoshiro Suzuki,
Yuki Furuichi,
Keiichiro Shiraga,
Hiroyuki Sasaki,
Azusa Ishida,
Sonoko Takahashi,
Takaharu Okada,
Kiminori Toyooka,
Jafar Sharif,
Takaya Abe,
Hiroshi Kanazawa,
Makoto Tominaga,
Atsushi Miyawaki,
Masayuki Amagai
Publication year - 2021
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.2020722118
Subject(s) - intracellular , corneocyte , keratinocyte , microbiology and biotechnology , stratum corneum , programmed cell death , biophysics , stratum granulosum , biology , chemistry , biochemistry , apoptosis , in vitro , genetics
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 Ca2+ 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.