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The loss of cell volume without a change in overall length suggests that cortical fiber compaction occurred as a result of compression along the equatorial plane rather than along the polar axis as seen in nuclear regions.
Together, the reduction in GFP and concomitant loss of cell volume suggest that ICAM-3 levels are unlikely to be reduced simply as a result of ICAM-3 cleavage from the cell, leaving behind the GFP tag and transmembrane domain.
Loss of AQP4 and AQP1 could represent a protective mechanism whereby astrocytes restrict water loss and prevent the triggering of apoptosis precipitated by a loss of cell volume [ 40, 43- 49].
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Necrosis is morphologically characterized by increasing of cell volume, dilation of organelles, rupture of the plasma membrane and subsequent loss of intracellular contents.
Necrosis is a type of cell death which is morphologically characterized by increase of cell volume, dilation of organelles, rupture of the plasma membrane and subsequent loss of intracellular contents.
VRAC opening causes compensatory loss of K+, Cl−, and excitatory amino acids including glutamate, accompanied by water, leading to recovery of cell volume.
Exponential growth of cell volume.
The basic mechanism of necrosis is thought to be a loss of control over cell volume, related to changes in the permeability of the cell membrane.
The end result is a decrease in cell volume without the loss of cell surface area, producing an EN with measurably shorter fiber cells with increased membrane complexity.
Unexpectedly, we also observed a JAG-dependent loss of coordination between cell volume and DNA synthesis, associated with increased heterogeneity in cell sizes.
In response, many if not all cells of the body are able to undergo a process of active adaptation accomplished by the extrusion of intracellular organic osmolytes in order to induce water loss and restore cell volume [ 29].
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