Inhibition of Osteocyte Membrane Repair Activity via Dietary Vitamin E Deprivation Impairs Osteocyte Survival.

Osteocytes experience plasma membrane disruptions (PMD) that initiate mechanotransduction both in vitro and in vivo in response to mechanical loading, suggesting that osteocytes use PMD to sense and adapt to mechanical stimuli. PMD repair is crucial for cell survival; antioxidants (e.g.

Mechanical loading disrupts osteocyte plasma membranes which initiates mechanosensation events in bone.

Osteocytes sense loading in bone, but their mechanosensation mechanisms remain poorly understood. Plasma membrane disruptions (PMD) develop with loading under physiological conditions in many cell types (e.g.

Difference in Membrane Repair Capacity Between Cancer Cell Lines and a Normal Cell Line.

Electroporation-based treatments and other therapies that permeabilize the plasma membrane have been shown to be more devastating to malignant cells than to normal cells. In this study, we asked if a difference in repair capacity could explain this observed difference in sensitivity. Membrane repair was investigated by disrupting the plasma membrane using laser followed by monitoring fluorescent dye entry over time in seven cancer cell lines, an immortalized cell line, and a normal primary cell line.

The antioxidant requirement for plasma membrane repair in skeletal muscle.

Vitamin E (VE) deficiency results in pronounced muscle weakness and atrophy but the cell biological mechanism of the pathology is unknown. We previously showed that VE supplementation promotes membrane repair in cultured cells and that oxidants potently inhibit repair. Here we provide three independent lines of evidence that VE is required for skeletal muscle myocyte plasma membrane repair in vivo.

Promotion of plasma membrane repair by vitamin E.

Severe vitamin E deficiency results in lethal myopathy in animal models. Membrane repair is an important myocyte response to plasma membrane disruption injury as when repair fails, myocytes die and muscular dystrophy ensues. Here we show that supplementation of cultured cells with α-tocopherol, the most common form of vitamin E, promotes plasma membrane repair.

A novel cellular defect in diabetes: membrane repair failure.

Objective: Skeletal muscle myopathy is a common diabetes complication. One possible cause of myopathy is myocyte failure to repair contraction-generated plasma membrane injuries. Here, we test the hypothesis that diabetes induces a repair defect in skeletal muscle myocytes.

Requirement for annexin A1 in plasma membrane repair.

Ca2+ entering a cell through a torn or disrupted plasma membrane rapidly triggers a combination of homotypic and exocytotic membrane fusion events. These events serve to erect a reparative membrane patch and then anneal it to the defect site. Annexin A1 is a cytosolic protein that, when activated by micromolar Ca2+, binds to membrane phospholipids, promoting membrane aggregation and fusion.

Yolk granule tethering: a role in cell resealing and identification of several protein components.

Homotypic fusion among echinoderm egg yolk granules has previously been reconstituted in vitro, and shown to be a rapid, Ca2+-triggered reaction that can produce extremely large (>10 microm diameter) fusion products. We here show that, prior to Ca2+-triggered fusion, yolk granules in vitro, if isolated in an appropriate buffer, became tethered to one another, forming large aggregates of more than 100 granules. Granule washing with mildly chaotropic salt abolished this tethering reaction, and prevented Ca2+-triggered formation of the large fusion products characteristic of tethered granules.