Cell blebbing

Others have demonstrated that hyperoxia altered cultured bovine pulmonary arterial endothelial cells in such a way that they released more 6-keto-PGFjjj and LTB4 upon stimulation with Ca " ionophore. Again it is unclear whether the ultrastructural changes of the endothelial cells (bleb formation, decreased membrane barrier) facilitates influx and LTB4 synthesis or... 

Estacion, Mark, and William P. Schilling. "Maitotoxin-Induced Membrane Blebbing and Cell Death in Bovine Aortic Endothelial Cells." BMC Physiology 1 (2001) 2. 

Maintenance of organellar integrity Maintenance of ATP levels Maintenance of ion homeostasis Membrane surface blebbing Nuclear chromatin condensation/fragmentation Requires synthesis of death effector proteins Prevented by blocking steps in the death cascade Does not adversely affect neighbor cells... 

The steps of apoptosis are distinct from those of necrosis which is a nonprogramed form of cell death in response to injury, in which the cell swells and bursts, causing inflammation. Apoptosing cells form a tight sphere and their membranes undulate, resulting in bulges that form blebs. The nuclear membrane breaks, and endonucleases clip chromosomes where the DNA is exposed from protective proteins. This occurs at 180-base... 

Degeneration Mitochondrial permeability transition with membrane depolarization, cytochrome c release, and mitochondrial swelling and fragmentation activation of caspases and cell death pathway, endonuclease fragmentation of DNA with chromatin and nuclear condensation phosphatidyserine exposure on cell surface cytoskeletal disruption with membrane blebbing... 

Cytoskeleton injury blebbing, shrinkage in apoptosis increased size in mitosis nuclear size contraction with apoptosis and swelling with cell cycle inhibition... 

Because of the loss of ionic balance, the water content of the cell increases (swelling or hydropic degeneration and membrane blebs occur). 

Therefore, ATP levels will reach a point when the cell cannot survive, Ca2+ levels are too high, and the plasma membrane blebs and ruptures. 

This process is an early morphological change in cells often seen in isolated cells in vitro but also known to occur in vivo. The blebs, which appear before membrane permeability alters, are initially reversible. However, if the toxic insult is sufficiently severe and the cellular changes become irreversible, the blebs may rupture. If this occurs, vital cellular components may be lost and cell death follows. The occurrence of blebs may be due to damage to the cytoskeleton, which is attached to the plasma membrane as described above. The cause may be an increase in cytosolic Ca2+, interaction with cytoskeletal proteins, or modification of thiol groups (see below). 

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