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Membrane repair redux: redox of MG53

Nature Cell Biology volume 11, pages 7–9 (2009)Cite this article

Most cells can rapidly repair extensive tears in their plasma membrane, a response dependent on extracellular calcium. Entry of extracellular oxidants through a membrane disruption oxidizes and thus activates a newly discovered membrane repair protein, MG53, in skeletal muscle cells.

The long-term response (on a timescale of hours) of mammalian cells to injury by various kinds of extraneous, non-physiological insults, such as heating or exposure to toxic chemicals, has been widely studied and characterized at the molecular level. How cells respond rapidly (on a timescale of seconds) to plasma membrane disruption, an injury that threatens the afflicted cell with an equally rapid death, is less well understood. Biologically speaking, the response of mammalian cells to plasma membrane disruption is of great interest because it occurs under physiological conditions. For example, myofibres of normally contracting skeletal muscle are observed to frequently suffer plasma membrane disruptions, especially in high-force-generating, eccentric contractions1. Importantly, it has recently been shown that muscle wasting occurs when myofibres, due to a genetic defect, are incapable of repairing the membrane, as would be predicted if membrane injury is a physiological event that must be countered by specialized repair mechanisms2.

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Figure 1: A model for membrane repair.

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  1. Department of Cellular Biology and Anatomy, Paul McNeil is at the Medical College of Georgia, 1120 15th Street, CB 2816, Augusta, GA 30912-2000, USA pmcneil@mail.mcg.edu,

    Paul McNeil

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McNeil, P. Membrane repair redux: redox of MG53. Nat Cell Biol 11, 7–9 (2009). https://doi.org/10.1038/ncb0109-7

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