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Apoptosis

© David Olle

Apoptosis is the term for programmed cell death in which cells commit suicide. Apoptosis was coined by Scottish researchers in 1972 in order to distinguish the process from necrosis, another form of cell death. The two terms are of Greek origin, with necrosis meaning "make dead," while apoptosis means "dropping off." 1The processes are very different. Necrotic death occurs when a cell is severely injured. Typical features are swelling and rupture of the cell, followed by inflammation. During apoptosis, the dying cell shrinks and pulls away from its neighbors. The nucleus disintegrates, and blebs or small fragments appear on the cell surface. Langlois

Why should a cell commit suicide? It turns out that cell death is just as important for the body as cell growth. Examples of apoptosis that occur during normal body processes include the formation of the outer layer of skin, the inner mucosal lining of the intestine, and the endometrial lining of the uterus, which is sloughed off during menstruation. Cells that are damaged beyond repair could be hazardous to the body, so are eliminated by apoptosis. When a cell is infected with virus, it receives a self-destruct signal before it can manufacture more virus material. After a successful cell-mediated immune response to an infection, the cytotoxic T-lymphocytes must be destroyed. Otherwise, they could begin attacking body constituents, leading to autoimmune diseases such as lupus and rheumatoid arthritis. If there is irreparable damage to its DNA, the cell is sacrificed in order to prevent abnormal gene expression leading to cancer.

How is apoptosis regulated?

Whether a cell continues to survive or commits suicide depends upon a delicate balance among various signaling processes and regulatory molecules. Apoptosis can be triggered by signals that are either internal or external to the cell. 3

The interplay between bcl-2 and bax proteins is a key process in determining if apoptosis takes place. The two proteins have similarities in structure, so bax can prevent expression of bcl-2 by binding with it. Bcl-2 is found in the mitochondria, a cellular structure important for energy formation. Bcl-2 inhibits apoptosis by preventing the release of cytochrome c protein. When irreversible damage occurs to the cell, the p53 gene stimulates the formation of bax protein, which promotes apoptosis by releasing cytochrome c. This process results in the activation of caspase enzymes that kill the cell by breaking down its constituent proteins. In B-cell leukemia and lymphoma, there is a common chromosomal abnormality. The bcl-2 gene region on chromosome 18 is moved to the immunoglobulin heavy chain region on chromosome 14. Although normally responsible for the production of large amounts of antibodies, the fusion gene now produces excessive bcl-2 protein. This over expressed bcl-2 prevents apoptosis; so damaged cells survive and could progress to a cancerous growth.

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