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Name Lecturer Course Code Date “Cell Death” All organism are made up of millions of cells that perform different functions under different conditions in their daily activities. These cells are subject to the ‘use – disuse’ theory and as such, they die after some time…
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Download file to see previous pages This programmed cell death is called apoptosis; where cells deliberately destroy themselves. The events around the death are controlled by the nuclear genes. It begins with the breaking of the chromosomal DNA into fragments then the breakdown of the nucleus. Ultimately after time the cell shrinks and is fed on by the neighboring cells and macrophages. Cells that are damaged for some reason like DNA alteration or infection undergo programmed death. The process removes lethal cells which could lead to undesired mutation or viral spread. The cell might as well die for reasons like starvation, trauma, or asphyxiate. (Geoffrey and Robert, 97 ) Programmed cell death plays a very major role in maintaining the life and health of organisms. It is a normal part of embryonic development. For instance, the fingers and toes of a human are webbed when in the embryonic stage. Through cell death, the webbing is removed through apoptosis. The immune and nervous systems are also largely developed through the same process. (Wayne, 24) The process of apoptosis involves a variety of intra and extra cellular stimuli. When it is induced by extra-cellular factors, it is triggered by cell surface death receptors. These death receptors have cytoplasmic death domains (FADD and TRADD). They are typified by the tumor necrosis receptor superfamily which includes tumor necrosis factor receptor 1 (TNFR-1), TNF related apoptosis – inducing ligand recptor 1 (TRAILR-1), death receptor 3ectodermal dysplasia receptor (EDAR), nerve growth receptor and the cytotoxic T-cell proteins like perforin and granzyme-B. The FAS receptor is found on the surface of the cell (on the chromosome) and it leads to programmed cell death. Apoptosis uses it as a pathway. It also uses the mitochondrial pathway (Geoffrey and Cooper, 46) Apoptosis is driven by the impetus of enzymes from the regulated family proteolytic enzymes called caspases. Caspases are made up of upstream (initiator) caspases which are normally activated by death receptor signalosomes, casase 9, activated by the mitochondrial cytochrome derived apoptosome; downstream caspases (effectors) which cleave the involved proteins. Interaction with death receptor cytoplasmic death inducing signaling complexes that contain FAS-associating death domain activates caspases 2, 8 and 10. The receptors are activated by ligands involved in signaling cell death hence supporting cell selection, homeostasis, and morphogenesis and host defense (Carlo, 16) Death receptor ligands include Fas ligand, tumor necrosis factor alpha, NF-related apoptosis inducing ligand, TNF-related weak inducer of apoptosis, TNF-related molecule 1 and nerve growth factor. The ligand is a homotrimetic type II transmembrane protein of the TNF family. It induces apoptosis through trimetization hence playing an important role in the regulation of immune system. It also has a role in the progression of cancer. It is the Fas ligand that forms the death inducing signaling complex (DISC). Caspase-8 is released from DISC to the cytosol and it cleaves the other effector caspases. This leads to DNA degradation, membrane blebbing and other events that are associated with apoptosis. It is suggested that the extrinsic Fas pathway on its own can induce apoptosis in certain cell types. These cells are dubbed Type 1 cells and are characterized by the inability of the anti-apoptotic members of the Bcl-2 ...Download file to see next pagesRead More
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