Apoptosis, or programmed cell death, is actually a critical bodily process despite its seemingly formidable name. It is a sort of ‘cell suicide’, in which certain morphological changes occur within the cell and result in its destruction. It functions as a mechanism by which cells can fight off infection and starvation; if one cell is damaged or in danger, it sacrifices itself for the greater good of the organism by getting rid of itself through apoptosis. In addition, programmed cell death is an integral part of proper tissue development. During embryonic development, humans grow webbed fingers and toes; if it weren’t for apoptosis, we would retain those webs after birth, which is a condition known as syndactyly. Because cell death is in large part about keeping damage from spreading, it is not hard to see that apoptosis also aids in tumor suppression and cancer prevention.
One of the players in the apoptotic pathway is a receptor protein called CD95. When another protein, CD95L, binds to this receptor, a death inducing signaling complex (DISC) is formed. This, in turn, sets off a signaling cascade that eventually leads to cell apoptosis. While this may be beneficial in the case of fighting off invading pathogens and the like, what happens when the ‘death messenger’ response overshoots and ends up killing off cells that could otherwise be healed? Researchers explored this in the case of spinal cord injuries in mice. They found that CD95L sets off an inflammatory response that recruits macrophages to the site of injury and marks the injured cells for apoptosis. When CD95L was switched off, however, the mice were allowed to heal. Such a discovery could lead to more informed approaches to inflammatory and immune-related diseases.
Reference: Helmholtz Association of German Research Centres. "'Death Messenger' Molecule Causes Inflammation After Spinal Cord Injury, Prevents Healing." ScienceDaily 6 March 2010. 8 March 2010
Photo credit: Reproductive and Cardiovascular Disease Research Group. Can be found here.
Linda Le is a contributing writer on biomedical research to TuftScope for Spring 2010.
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