Delayed cell death signaling in traumatized central nervous system: hypoxia.
There are two different ways for cells to die: necrosis and apoptosis. Cell death has traditionally been described as necrotic or apoptotic based on morphological criteria. There are controversy about the respective roles of apoptosis and necrosis in cell death resulting from trauma to the central nervous system (CNS). An evaluation of work published since 1997 in which electron microscopy was applied to ascertain the role of apoptosis and necrosis in: spinal cord injury, stroke, and hypoxia/ischemia (H/I) showed evidence for necrosis and apoptosis based on DNA degradation, presence of histones in cytoplasm, and morphological evidence in spinal cord. In the aftermath of stroke, many of the biochemical markers for apoptosis were present but the morphological determinations suggested that necrosis is the major source of post-traumatic cell death. This was not the case in H/I where both biochemical assays and the morphological studies gave more consistent results in a manner similar to the spinal cord injury studies. After H/I, major factors affecting cell death outcomes are DNA damage and repair processes, expression of bcl-like gene products and inflammation-triggered cytokine production.
Chu
Danielle
D
Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston, USA.
Qiu
JingXin
J
Grafe
Marjorie
M
Fabian
Roderick
R
Kent
Thomas A
TA
Rassin
David
D
Nesic
Olivera
O
Werrbach-Perez
Karin
K
Perez-Polo
Regino
R
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D016923:Cell Death / Q000502:physiology; D002490:Central Nervous System / Q000098:blood supply*; D000860:Hypoxia / Q000503:physiopathology*; D007511:Ischemia / Q000503:physiopathology*; D009336:Necrosis; D009474:Neurons / Q000502:physiology*; D015398:Signal Transduction; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D020521:Stroke / Q000503:physiopathology*; D013997:Time Factors