Plasma membrane repair: the adaptable cell life-insurance

Ferroptotic pores induce Ca2+ fluxes and ESCRT-III activation to modulate cell death kinetics

“…The repair of plasma membrane damage induced by a variety of stimuli is an automatic response of the cell initiated by the acute and local increase in cytosolic Ca 2+ concentration, as a consequence of greater membrane permeability (Andrews & Corrotte, 2018, Jimenez & Perez, 2017. It has been previously reported that during necroptosis and pyroptosis membrane repair dependent on the action of the ESCRT-III complex delays cell death (Gong et al, 2017a, Gong et al, 2017b, Ruhl et al, 2018.…”

“…Damage to the plasma membrane in other forms of necrotic death like necroptosis (Cai, Jitkaew et al, 2014, Ousingsawat, Cabrita et al, 2017, Ros, Pena-Blanco et al, 2017, pyroptosis (de Vasconcelos, Van Opdenbosch et al, 2018, Ruhl, Shkarina et al, 2018, or upon chemical, toxin, or laser-induced cell death (Espiritu, Pedrera et al, 2019) results in the activation of ion fluxes. In these scenarios, Ca 2+ fluxes resulting from membrane damage have been linked with the activation of membrane repair mechanisms (Andrews & Corrotte, 2018, Etxaniz, Gonzalez-Bullon et al, 2018, Jimenez & Perez, 2017. The Endosomal sorting complexes required for transport (ESCRT) machinery seems to play a critical counterbalancing role that can delay or even block cell death in necroptosis and pyroptosis (Gong, Guy et al, 2017a, Gong, Guy et al, 2017b, Ruhl et al, 2018.…”

Mechanisms protecting host cells against bacterial pore-forming toxins

“…Its emergence was a critical event during evolution, and its integrity is crucial to maintain cellular homeostasis and support life [3]. Transient PM lesions still occur in healthy conditions, particularly, in tissues under high mechanical stress or biochemical stress such as muscle, skin, or gut epithelia [4, 5]. Conversely, persistent PM damage hallmarks several pathologies, such as heart failure, neurodegeneration, and infection [6–9].…”

“…In recent years, considerable advances were made regarding the identification and characterization of PM repair mechanisms and single-cell recovery processes. Such studies have highlighted the sequential nature that underlies the spatio-temporal coordination of cell recovery, but have predominantly focused on localized mechanical- or laser-induced damage (reviewed recently in [5, 25]). Accordingly, although the mechanisms identified are still relevant in the context of PFT-mediated damage, the specific features of repairing stable protein pores and recovering cellular homeostasis following PM damage caused by bacterial PFTs remain poorly understood.…”

Imaging Membrane Repair in Single Cells Using Correlative Light and Electron Microscopy

“…Chemical treatment is based on the use of detergent (McNeil et al., ) or pore‐forming toxins such as streptolysin‐O (Babiychuk et al., ). These treatments form small pores (<100 nm) on the overall plasma membrane surface, whereas mechanical injury leads to larger (from 100 nm to few µm) and less numerous or unique wounds (Jimenez & Perez, ). Mechanical injury methods include the use of a needle (Terasaki et al., ), mechanical shearing (McNeil & Baker, ) or stretching (Yasuda et al., ), or laser irradiation (Bansal et al., ; Bouter et al., ; Clarke, Caldwell, Chiao, Miyake, & McNeil, ; Koerdt & Gerke, ; McNeil, Miyake, & Vogel, ).…”