Plasma Membrane Repair: A Central Process for Maintaining Cellular Homeostasis

Blazek, Alisa D.; Paleo, Brian J.; Weisleder, Noah

doi:10.1152/physiol.00019.2015

Cited by 95 publications

(89 citation statements)

References 140 publications

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“…These MG53-containing vesicles then form a membrane patch to repair the damaged sarcolemma. Evidence also suggests that caveolin-3 is involved in MG53-mediated membrane repair [36]. Caveolin-3 co-localizes and interacts with MG53 and dysferlin, thereby regulating MG53 activity such as MG53-mediated membrane fusion events [32].…”

Section: Discussionmentioning

confidence: 99%

MG53 is dispensable for T-tubule maturation but critical for maintaining T-tubule integrity following cardiac stress

Zhang

Chen

Wang

et al. 2017

Journal of Molecular and Cellular Cardiology

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The cardiac transverse (T)-tubule membrane system is the safeguard for cardiac function and undergoes dramatic remodeling in response to cardiac stress. However, the mechanism by which cardiomyocytes repair damaged T-tubule network remains unclear. In the present study, we tested the hypothesis that MG53, a muscle-specific membrane repair protein, antagonizes T-tubule damage to protect against maladaptive remodeling and thereby loss of excitation-contraction coupling and cardiac function. Using MG53-knockout (MG53-KO) mice, we first established that deficiency of MG53 had no impact on maturation of the T-tubule network in developing hearts. Additionally, MG53 ablation did not influence T-tubule integrity in unstressed adult hearts as late as 10 months of age. Following left ventricular pressure overload-induced cardiac stress, MG53 protein levels were increased by approximately three-fold in wild-type mice, indicating that pathological stress induces a significant upregulation of MG53. MG53-deficient mice had worsened T-tubule disruption and pronounced dysregulation of Ca2+ handling properties, including decreased Ca2+ transient amplitude and prolonged time to peak and decay. Moreover, MG53 deficiency exacerbated cardiac hypertrophy and dysfunction and decreased survival following cardiac stress. Our data suggest MG53 is not required for T-tubule development and maintenance in normal physiology. However, MG53 is essential to preserve T-tubule integrity and thereby Ca2+ handling properties and cardiac function under pathological cardiac stress.

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Section: Discussionmentioning

confidence: 99%

MG53 is dispensable for T-tubule maturation but critical for maintaining T-tubule integrity following cardiac stress

Zhang

Chen

Wang

et al. 2017

Journal of Molecular and Cellular Cardiology

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“…The disruption of the sarcolemma triggers the recruitment of vesicles to the injury site by a muscle‐specific protein, Mitsugumin‐53 (MG53). Dysferlin play a major role in fusing these vesicles to form a membrane repair patch . Anoctamin‐5 has been recently shown to be critical for membrane repair, but how it functions in the membrane repair complex remains unknown …”

Section: Lgmd Subgroupsmentioning

confidence: 99%

“…There is emerging evidence that caveolae also are a part of the membrane repair complex . Only CAV3 mutations that cause retention of MG53 and dysferlin in the Golgi apparatus result in secondary membrane repair defects .…”

Section: Lgmd Subgroupsmentioning

confidence: 99%

Untangling the complexity of limb‐girdle muscular dystrophies

Liewluck

Milone

2018

Muscle and Nerve

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The limb-girdle muscular dystrophies (LGMDs) are a group of genetically heterogeneous, autosomal inherited muscular dystrophies with a childhood to adult onset, manifesting with hip- and shoulder-girdle muscle weakness. When the term LGMD was first conceptualized in 1954, it was thought to be a single entity. Currently, there are 8 autosomal dominant (LGMD1A-1H) and 26 autosomal recessive (LGMD2A-2Z) variants according to the Online Mendelian Inheritance in Man database. In addition, there are other genetically identified muscular dystrophies with an LGMD phenotype not yet classified as LGMD. This highlights the entanglement of LGMDs, which represents an area in continuous expansion. Herein we aim to simplify the complexity of LGMDs by subgrouping them on the basis of the underlying defective protein and impaired function. Muscle Nerve 58: 167-177, 2018.

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“…However, nearly a century ago the requirement of calcium for repairing injured cells was first reported by way of a “surface precipitation reaction” [42,7]. Excessive calcium entry across the plasma membrane is a universal signal to trigger the plasma membrane repair response [3–5]. A critical element of the calcium-triggered repair response is the cell’s ability to switch it off by removing excess cytosolic calcium.…”

Section: Signals and Effectors Of Plasma Membrane Repairmentioning

confidence: 99%

“…This explains the need for a ubiquitous pathway to repair plasma membrane injury in all cells. Plasma membrane repair has been studied in a wide variety of organisms and cell types and defects in plasma membrane repair have been identified in a growing number of diseases associated with tissue degeneration (reviewed in [3–5]). Despite the capacity of all cells to repair their plasma membrane, all cells do not experience similar injuries.…”

mentioning

confidence: 99%

Cellular mechanisms and signals that coordinate plasma membrane repair

Horn

Jaiswal

2018

Cell. Mol. Life Sci.

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Plasma membrane forms the barrier between the cytoplasm and the environment. Cells constantly and selectively transport molecules across their plasma membrane without disrupting it. Any disruption in the plasma membrane compromises its selective permeability and is lethal, if not rapidly repaired. There is a growing understanding of the organelles, proteins, lipids, and small molecules that help cells signal and efficiently coordinate plasma membrane repair. This review aims to summarize how these subcellular responses are coordinated and how cellular signals generated due to plasma membrane injury interact with each other to spatially and temporally coordinate repair. With the involvement of calcium and redox signaling in single cell and tissue repair, we will discuss how these and other related signals extend from single cell repair to tissue level repair. These signals link repair processes that are activated immediately after plasma membrane injury with longer term processes regulating repair and regeneration of the damaged tissue. We propose that investigating cell and tissue repair as part of a continuum of wound repair mechanisms would be of value in treating degenerative diseases.

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Plasma Membrane Repair: A Central Process for Maintaining Cellular Homeostasis

Cited by 95 publications

References 140 publications

MG53 is dispensable for T-tubule maturation but critical for maintaining T-tubule integrity following cardiac stress

MG53 is dispensable for T-tubule maturation but critical for maintaining T-tubule integrity following cardiac stress

Untangling the complexity of limb‐girdle muscular dystrophies

Cellular mechanisms and signals that coordinate plasma membrane repair

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