proteinkinasecanditsinvolvementinpathophysiologicdisorders-文庫(kù)吧資料
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【正文】 ublethal ischemic episode, the brain enacts endogenous neuroprotective mechanisms to induce tolerance, rendering it protected against a subsequent lethal transient ischemic attack. ? early preconditioning ? delayed preconditioning The activation or translocation of PKC in the central nervous system may play a key role in mediating both early and delayed preconditioning. Email: Email: Email: Email: Gene transcription, Protein synthesis P P PKCβⅡ , γ, ε mGluR Early HPC Delayed HPC Hypoxia NMDAR AR PLC α γ β PIP2 IP3 DAG Ca2+ ER K+ATP channel ERK JNK p38 P P P P P P MAPK α, βI, βII, γ δ, ε, ε, ζ δ, η/λ PKC TykR Unknown ? Glutamate Adenosine Po2 MSK, RSK, Ng… P P P Known glucose ATP Email: PKC amp。36:27812790. Email: Stroke. 20xx。36:27812790. Email: ?Release of cytochrome C promotes apoptosis through the activation of caspases and subsequent DNA damage events in the nucleus. Stroke. 20xx。24:6880–6888.) Email: ?Reperfusion injury contributes to detrimental cell signaling, in part via release of glutamate and free radicals from the ischemic core and the recruitment of inflammatory mediators. Stroke. 20xx。20:93–102.) ?nPKC? levels are increased in the perifocal region during reperfusion, suggesting a role for this enzyme in mediating delayedinjury processes. (J Neurosci. 1996。36:27812790. Email: ?cPKC? may potentiate NMDAR function via Src tyrosine kinases. This feedback mediates increases in intracellular calcium, leading to mitochondrial dysfunction, ROS formation, and cell death. Stroke. 20xx。20:343–349) Email: ?Ischemiainduced reduction in blood oxygen and glucose delivery to the brain causes reduction in cellular ATP levels, leading to deregulation of cellular ion pumps and loss of intracellular ion homeostasis. Stroke. 20xx。44:105–109) ? cPKC? is activated specifically during reperfusion. (J Cereb Blood Flow Metab. 20xx。36:27812790. Email: ? nPKC? induce opening of K (ATP) channels in the mitochondria, maintain ATP production and reduce generation of ROS. nPKC? leads to activation of ERK, which is involved in antiapoptotic signaling and cell survival. Stroke. 20xx。 47:136 –145) Email: ?Preconditioning stimuli, including hypoxia, lead to a decrease in cellular ATP stores and the subsequent generation of adenosine, A1/A3 adenosine receptors (ARs) activate PLC via Gproteins. Stroke. 20xx。23:384 –391) ? Delivery of an nPKC? specific activator peptide before OGD reduces damage, in pure neuronal and mixed neuronal/astrocyte cultures. (Neuropharmacology. 20xx。 Cerebral Ischemia/ Reperfusion Injury PKC Involved in Pathophysiologic Disorders Email: ?Ischemic core ? Distal to an occluded artery, undergoes rapid, anoxic cell death within minutes. ? Irreversible processes: mitochondrial collapse, rapid energy depletion, and ion pump failure result in large increases in intracellular calcium, extracellular potassium, and edematous cell swelling, characteristic of necrotic cell death ?
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