2012, Número S1
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Rev Med UV 2012; 12 (S1)
Necrosis Neuronal Programada
López-Meraz ML, Juárez-Aguilar E, Medel-Matus JS, Álvarez CDM, Galán ZR, Pérez ECA, Hernández ME, Miquel M, Manzo J
Idioma: Español
Referencias bibliográficas: 36
Paginas: 17-22
Archivo PDF: 425.13 Kb.
RESUMEN
Desde el punto de vista morfológico, la muerte celular se ha
clasificado en numerosos tipos, siendo los principales la necrosis,
caracterizada por la ruptura de la membrana plasmática y el
hinchamiento de organelos, y la apoptosis, en la que se observa
condensación nuclear mientras la membrana celular se encuentra
intacta. Tradicionalmente, la apoptosis se ha denominado muerte
celular programada, ya que se relaciona con la ejecución de un
mecanismo intracelular orquestado que implica la expresión
génica, la síntesis de proteínas y activación de caspasas. En
cambio, la necrosis, se asume como un mecanismo pasivo que se
genera por la entrada masiva de iones y agua al interior celular.
Sin embargo, evidencia actual apunta a la existencia de muerte
celular con morfología necrótica, pero cuya génesis implica la
ejecución regulada de eventos intracelulares. Específicamente
para el caso de las neuronas, este tipo de necrosis “activa” se
ha observado en ciertas condiciones experimentales y se ha
denominado ya sea “necrosis programada” ó “necroptosis”,
dependiendo del mecanismo de señalización involucrado. El
objetivo de esta revisión es describir el conocimiento actual
sobre estas formas de necrosis neuronal con énfasis en los
mecanismos de la “necrosis programada”.
REFERENCIAS (EN ESTE ARTÍCULO)
Kroemer G y col. Classification of cell death: recommendations of the Nomenclature Committee on Cell Death. Cell Death Differ. 2009; 16(1): 3–11.
Li Y y col. Induction of DNA fragmentation after 10 to 120 minutes of focal cerebral ischemia in rats. Stroke 1995; 26(7):1252-8.
Lopez-Meraz ML, Niquet J, Wasterlain CG. Distinct caspase pathways mediate necrosis and apoptosis in subpopulations of hippocampal neurons after status epilepticus. Epilepsia 2010; 51 (Suppl 3): 56-60.
Nagley P, Higgins GC, Atkin JD, Beart PM. Multifaceted deaths orchestrated by mitochondria in neurones. Biochim Biophys Acta 2010; 1802(1):167-85.
Wyllie AH. Cell death: a new classification separating apoptosis from necrosis. In Cell Death in Biology and Pathology. Bowen, I.D. and Lockshin, R.A, (Eds.). Chapman and Hall, London. 1981.
Kerr JFR, Wyllie AH, Currie AR. Apoptosis: a basic biological phenomenon with wideranging implications in tissue kinetics. Br J Cancer 1972; 26:239-257.
Galluzzi L y col. Cell death modalities: classification and pathophysiological implications. Cell Death Differ 2007; 14:1237-43.
Golstein P, Kroemer G. Cell death by necrosis: towards a molecular definition. Trends Biochem Sci 2007; 32(1):37-43.
Liou AKF y col. To die or not to die for neurons in ischemia, traumatic brain injury and epilepsy: a review on the stress-activated signaling pathways and apoptotic pathways. Prog Neurobiol 2003; 69:103- 142.
Li P y col. Cytochrome c and dATP-dependent formation of APAf-1/ caspase-9 complex initiates an apoptotic protease cascade. Cell 1997; 91:479-489.
Bao Q, Shi Y. Apoptosome: a platform for the activation of initiator caspases. Cell Death Differ 2007; 14:56-65
Niquet J, Wasterlain CG. Bim, Bad and Bax: a deadly combination in epileptic seizures. J Clin Invest 2004; 113:960-962.
Henshall DC, Murphy BM. Modulators of neuronal cell death in epilepsy. Curr Opin Pharmacolol 2008; 8:75-81.
Niquet J y col. Hypoxic neuronal necrosis: protein synthesisindependent activation of a cell death program. Proc Natl Acad Sci USA 2003; 100:2825-30.
Niquet J, Seo DW, Wasterlain CG. Mitochondrial pathways of neuronal necrosis. Biochem Soc Trans 2006; 34:1347-51.
Seo DW y col. Contribution of a mitochondrial pathway to excitotoxic neuronal necrosis. J Neurosci Res 2009; 78(4-5):131.
Niquet J, Seo DW, Allen SG, Wasterlain CG. Hypoxia in presence of blockers of excitotoxicity induces a caspase-dependent neuronal necrosis. Neuroscience 2006; 141(1):77-86.
Chen JW, Naylor DE, Wasterlain CG. Advances in the pathophysiology of status epilepticus. Acta Neurol Scand Suppl 2007; 186:7-15.
Wasterlain CG, Shirasaka Y. Seizures, brain damage and brain development. Brain Dev. 1994; 16(4):279-95.
Tokuhara D y col. Kainic acid dose affects delayed cell death mechanism after status epilepticus. Brain Dev 2007; 29:2-8.
Carloni S, Carnevali A, Cimino M, Balduini W. Extended role of necrotic cell death after hypoxia-ischemia-induced neurodegeneration in the neonatal rat. Neurobiol Dis 2007; 27:354-61.
Niquet J y col. Status Epilepticus Triggers Caspase-3 Activation and Necrosis in the Immature Rat Brain. Epilepsia 2007; 48:1203-6.
Lopez-Meraz ML y col. Vulnerability of postnatal hippocampal neurons to seizures varies regionally with their maturational stage. Neurobiol Dis 2010; 37:394-402.
Harris KM, Teyler TJ. Developmental onset of long-term potentiation in area CA1 of the rat hippocampus. J Physiol 1984; 346:27-48.
Bekenstein JW, Lothman EW. An in vivo study of the ontogeny of longterm potentiation (LTP) in the CA1 region and in the dentate gyrus of the rat hippocampal formation. Brain Res Dev Brain Res 1991; 63:245-251.
Bekenstein JW, Lothman EW. A comparison of the ontogeny of excitatory and inhibitory neurotransmission in the CA1 region and dentate gyrus of the rat hippocampal formation. Brain Res Dev Brain Res 1991; 63:237-243.
Vekrellis K y col. Bax promotes neuronal cell death and is downregulated during the development of the nervous system. Development 1997; 124(6):1239-49.
Yakovlev AG y col. Differential expression of apoptotic proteaseactivating factor-1 and caspase-3 genes and susceptibility to apoptosis during brain development and after traumatic brain injury. J Neurosci 2001; 21(19):7439-46.
López-Meraz ML y col. El status epilepticus induce la expresión de la interleucina-1β en el cerebro de la rata en desarrollo. LIV Congreso Nacional de Ciencias Fisiológicas; 2011 Sep 10-14; León, Guanajuato, México.
Álvarez-Croda DM y col. Interleukin-1 beta expression in hippocampus following status epilepticus in the developing rat. SfN’s Annual meeting of Neuroscience; 2011 Nov 12-16; Washington DC, USA.
Degterev A y col. Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury. Nat Chem Biol 2005 Jul; 1(2):112-9.
Christofferson D, Yuan J. Necroptosis as an alternative form of programmed cell death. Curr Opin Cell Biol 2010; 22(2): 263-268.
Galluzzi L, Kroemer G. Necroptosis: a specialized pathway of programmed necrosis. Cell 2008; 135(7):1161-3.
Li Y y col. Necroptosis contributes to the NMDA-induced excitotoxicity in rat’s cultured cortical neurons. Neurosci Lett 2008; 447(2- 3):120-3.
Chen Y. Necrosis: an energy dependent programmed cell death? UTMJ 2009; 86(3):110-112.
You Z y col. Necrostatin-1 reduces histopathology and improves functional outcome after controlled cortical impact in mice. J Cereb Blood Flow Metab 2008; 28(9):1564-73.