Following the TRAIL to apoptosis |
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Authors: | Chaudhari Bharti R Murphy Richard F Agrawal Devendra K |
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Institution: | (1) Department of Biomedical Sciences, Creighton University School of Medicine, Room 510, 68178 Omaha, NE |
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Abstract: | Apoptosis, programmed cell death, eliminates injured or harmful cells. It can mediate its response through the actions of
death ligands including TRAIL. TRAIL, a member of TNF superfamily, induces apoptosis of transformed cells through the action
of death domain receptors DR-4 and DR5. It directly induces apoptosis through an extrinsic pathway, which involes the activation
of caspases. TRAIL also is able to prevent apoptosis through the actions of its decoy receptors DcR-1 and DcR-2. Various regulators
of TRAIL include FADD, IAPs, Bcl-2s, p53, and FLIPs. TRAIL is present in cells involved in asthma including eosinophils, mast
cells, fibroblasts, and airway epithelial cells. It is expressed in airway remodeling and may be linked with the pathways
of transforming growth factor-beta1, which is thought to cause damage to the epithelium. The repair process of the epithelium
is hindered as a result of increased apoptosis induced by TGF-β1, which overlaps with the pathways of TRAIL. Analogs of TRAIL
could have therapeutical applications for asthma. TRAIL is also seen as the basis for a “miracle” drug for cancer because
of its ability to selectively kill cancer cells. |
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Keywords: | Airway remodeling Apoptosis Asthma Regulators of TRAIL TGF-β 1 TRAIL TRAIL receptors |
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