Plasma membrane repair

Abstract

Tissue wound repair has been studied extensively. It involves the coordinated activation of several intracellular and intercellular pathways, as well as remodeling from the sequential recruitment of different cell types to the wound site. There is, however, an equally important process that happens at the single cell level, when the integrity of the plasma membrane is compromised. Individual eukaryotic cells can rapidly repair their plasma membrane after injury, through a process that restores internal homeostasis and prevents cell death. Despite its importance, investigations of this fascinating mechanism have been limited. Only recently have we begun to understand that plasma-membrane repair resembles tissue healing, in the sense that it also involves sequential, highly localized remodeling steps that ultimately eliminate all traces of the injury.

Mechanisms protecting host cells against bacterial pore-forming toxins

“…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.…”

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

“…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.…”

Low dose Cold Atmospheric Plasma induces membrane oxidation, stimulates endocytosis and enhances uptake of nanomaterials in Glioblastoma multiforme cells

“…The Streptolysin O, to create mechanical injuries on membranes 45 . Meanwhile, lipid peroxidation is a complex process that damages cellular membrane structure and function, which is believed to link to numerous human diseases and aging, including Alzheimer diseases, dementia, Huntington, Parkinson, and traumatic injuries, under presence of oxidative stress 48,49 .…”

“…A membrane repair mechanism has been described for cells 44,45 . Through rapid endocytosis, cells can quickly remove damaged regions of membranes from the cell surface.…”