Apoptosis ischemic

Hypoxia-ischemia may initiate apoptosis in parallel with excitotoxicity 565 Triggers of ischemic apoptosis may include decreased supply or sensitivity to neurotrophins, oxidative stress, exposure to inflammatory cytokines or damage to mitochondria 566... 

D1 (10,17S-docosatriene) from DHA using tandem liquid chromatography-photodiode array-electrospray ionization-tandem mass spectrometry (LC-PDA-ESI-MS-MS)-based lipidomic analysis have been documented in ischemic brain [4] and retinal pigment epithelium [5], This new lipid is called neuroprotectin D1 (1) because of its neuro-protectiveproperties in brain ischemia-reperfusion [4] and in oxidative stress-challenged retinal pigment epithelial cells [5] (2) because of its potent ability to inactivate proapoptotic signaling (see apoptosis, Ch. 35) [5] and (3) because it is the first identified neuroprotective mediator derived from DHA. 

Bcl-2 B cell lymphoma protein 2 (Bcl-2) is a family of proteins that regulate apoptosis (programmed cell death). Apoptosis is a necessary process whereby aged or damaged cells are replaced by new cells. Dysfunction of the apoptosis process results in disease inhibition of apoptosis results in cancer, autoimmune disorder, and viral infection, whereas increased apoptosis gives rise to neurodegenerative disorders, myelodysplastic syndromes, ischemic injury, and toxin-induced liver disease. 

Cao G, Pei W, Ge H, et al. In vivo delivery of a Bcl-xL fusion protein containing the TAT protein transduction domain protects against ischemic brain injury and neuronal apoptosis. J Neurosci 2002 22(13) 5423-5431. 

Kocher, A.A., Schuster, M.D., Szabolcs, M.J., Takuma, S., Burkhoff, D., Wang, J., Homma, S., Edwards, N.M. and Itescu, S. (2001). Neovascularization of ischemic myocardium by human bone marrow derived angioblasts prevents cardiomyoc34e apoptosis, reduces remodeling and improves cardiac function. Nat Med 7, 430-446. 

Molecular imaging may potentially address not only the pathophysiology of ischemia but also vascular inflammation causing rupture of atherosclerotic plaques before major ischemic events. Initial approaches have used imaging of "indium radiolabeled monocytes [150], upregulated metallo-proteinases [151], and imaging of apoptosis in atherosclerotic lesions [152]. However, none have evolved into clinically useful tests. 

The main differences between necrosis and apoptosis are in the triggers (accidental v. physiological), the process (energy-independent vs. dependent), and the outcomes (with vs. without inflammation). However, apoptosis and/or necrosis can be induced by the same causes in some cases (K16). Alteration of mitochondrial permeability is involved in both apoptosis and necrosis (K16). Both apoptosis and necrosis are found in conditions such as stroke and myocardial infraction (F5), and necrosis can occur secondary to apoptosis (T4). To preserve the usefulness of the two terms for denoting different modes of cell death while still recognizing possible overlap of the two processes (H7), some more descriptive terms have been proposed primary necrosis (oncosis, ischemic cell death) (Ml) and secondary necrosis (apoptotic necrosis, necrosis secondary to apoptosis) (K15). 

Benzodiazepin-2-one Y demonstrates anti-ischemic activity in vitro protecting neuronal cell from apoptosis and necrosis, with the (V)-isomer more active than the (iJ)-isomer <2007BML1326>. 

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