Interleukin mitochondrial

Calcium oxalate monohydrate responsible for the formation of most kidney stones significantly increased mitochondrial superoxide production in renal epithelial cells [42], Recombinant human interleukin IL-(3 induced oxygen radical generation in alveolar epithelial cells, which was suppressed by mitochondrial inhibitors 4 -hydroxy-3 -methoxyacetophe-none and diphenylene iodonium [43]. Espositio et al. [44] found that mitochondrial oxygen radical formation depended on the expression of adenine nucleotide translocator Anti. Correspondingly, mitochondria from skeletal muscle, heart, and brain from the Antl-deficient mice sharply increased the production of hydrogen peroxide. 

Fas ligand and interleukin-ip), the neurotransmitter glutamate and thrombin. Like tumor necrosis factor (TNF) receptors, Fas is coupled to downstream death effector proteins that ultimately induce caspase activation (Ch. 22). Fas and TNF receptors recruit proteins called FADD and TRADD respectively FADD and TRADD then activate caspase-8, which, in turn, activates caspase-3 (Fig. 35-4). Calcium ion influx mediates neuronal apoptosis induced by glutamate receptor activation calcium induces mitochondrial membrane permeability transition pore opening, release of cytochrome c and caspase activation. Interestingly, in the absence of neurotrophic factors some neurotrophic factor receptors can activate apoptotic cascades, the low-affinity NGF receptor being one example of such a death receptor mechanism [23],... 

Fig. 1. Proposed mechanism of action of rituximab associated with the apoptosis pathway. Binding of rituximab with the CD20 antigen up-regulates the production of interleukin-10 (IL-10). The IL-10 autocrine loop down-regulates the expression of the bcl-2 protein, which inhibits the intrinsic pathway (or mitochondrial mediated pathway) of apoptosis. The mitochondrial pathway is induced by intracellular stress signals. The translocation of the bcl-2 protein into the mitochondria leads to the activation of caspase 9 via release of cytochrome c and apoptotic protease-activating factor 1. The other pathway, the extrinsic pathway (or death receptor mediated pathway) activates caspase 8. Subsequently, caspase 8 or 9 activates caspase 3, leading to programmed cell death (apoptosis).

Sandler, S., Bendtzen, K., Hakan Borg, L. A., Eizirik, D. L., Stranded, W., and Welsh, N. (1989). Studies on the mechanisms causing inhibition of insulin secretion in rat pancreatic islets exposed to human interleukin-1/3 indicate a perturbation in the mitochondrial function. Endocrinology (Baltimore) 124, 1492-1501. 

Lemasters JJ (1998) The mitochondrial permeability transition from biochemical curiosity to pathophysiological mechanism. Gastroenterology 115 783-786 Li W, Liang X, Leu JI, Kovalovich K, Ciliberto G, Taub R (2001) Global changes in interleukin-6-dependent gene expression patterns in mouse livers after partial hepatectomy. Hepatology... 

Fig. 1. Modulation of apoptosis by v-FLIP and v-Bcl-2. v-FLIPs specifically inhibit apoptosis mediated by death receptors. v-lCA specifically targets caspase-8 and inhibits its activation. v-Bcl-2 and vMIA inhibit those apoptotic pathways that are signaled through mitochondrial release of cytochrome c. FADD, Fas-associated death domain FLICE, FADD-like interleukin-converting enzyme CARD, cas-pase-recruiting domain PTPC. permeability transition pore complex FLIP, FLICE-inhibitory protein vie A, viral inhibitor of caspase 8-induced-apoptosis MIA. viral mitochondrial inhibitor of apoptosis Apcif-l, apoptotic protease-activating factor 1...

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