from PART II - ENDOTHELIAL CELL AS INPUT-OUTPUT DEVICE
Published online by Cambridge University Press: 04 May 2010
In an article published by Kerr and colleagues in 1972, the term apoptosis, defined as “dropping off or falling off of … leaves from trees,” was used to describe energy-dependent cellular suicide with distinct morphologic characteristics, such as chromatin condensation, plasma membrane blebbing, and apoptotic body formation (1). The term apoptosis, however was first used in medicine by Hippocrates (460–370 B.C.) to describe the “falling off of the bones” in a book discussing bone fractures (2). The term was also reportedly utilized by Galen (129–201 A.D.) to describe the “dropping of the scabs” (2). Since the re-introduction of apoptosis to scientific and medical literature 33 years ago, close to 95,000 articles published and listed in National Library of Medicine's PubMed make use of the term.
Apoptosis or programmed cell death describes a genetically determined elimination of cells that are in excess, injured, infected, or aged. Once committed to programmed suicide, cells undergo well-ordered morphologic and molecular alterations, including cytoskeletal rearrangement, nuclear membrane collapse, chromatin condensation, cell shrinkage, plasma membrane blebbing, and the formation of disassembled membrane-enclosed vesicles, referred to as apoptotic bodies (1). DNA fragmentation also occurs by activated endonucleases, resulting in the cleavage of genomic DNA into 180- to 200-base pair fragments (1). Additionally, phosphatidylserine exposure at the cell surface acts as a chemoattractant for macrophages, thus promoting the engulfment of these apoptotic bodies and the prevention of inflammation due to limited release of intracellular contents (3,4). In contrast, cells undergoing necrosis swell and lyse, thereby releasing intracellular contents into the interstitium, leading to an inflammatory response (5).
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