"The cells lose their all-important external boundaries," Dr. McNeil said. The result is that calcium B present outside these cells at concentrations10,000 times higher than intracellular levels B rushes in to promote healing or wreak destruction.
"It's a paradox," Dr. McNeil said. Inside muscle cells, the normal, low levels of calcium signal muscle contraction. In studies first done in sea urchins and fibroblasts, Dr. McNeil documented that when extracellular calcium rushes in through a tear in the cell membrane, it can either help form the cell-saving patch or destroy the cell, possibly by prompting the cell to contract to death.
"In a sea urchin egg, you can rip off 1,000 square microns of surface, the equivalent of one-third of the surface of the egg and, within seconds, no more calcium is coming in," Dr. McNeil said. "There is complete restoration of the surface covering of the egg within seconds.
The egg can then be fertilized and go on to divide; so afterward, it's healthy," he said of research findings first published in Journal of Cell Biology and Journal of Cell Science; a review article is scheduled for the May issue of Nature Cell Biology.
The cell-saving patch results from a fusion of vesicles, little spherical structures that normally nourish the cell, and the initial onslaught of external calcium. "The calcium that rushes in through the membrane disruption causes small vesicles or membranes inside the cells, to fuse with each other, making a bigger membrane structure that is a patch," Dr. McNeil said. "The patch then fuses with the cell surface."
But if that patch doesn't form, calcium continues to rush in, rapidly becoming the villain by killing off some of the finite number of muscle cells. "If you inhibit this (patching) process, within less than a minute, the cell will be dead," Dr. McNeil said.
With the three-year, nearly $900,000 grant fr
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Contact: Toni Baker
tbaker@mail.mcg.edu
706-721-4421
Medical College of Georgia
17-Apr-2001