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Willoughby KA Kleindienst A Müller C Chen T Muir JK Ellis EF 《Journal of neurochemistry》2004,91(6):1284-1291
S100B protein in brain is produced primarily by astrocytes, has been used as a marker for brain injury and has also been shown to be neurotrophic and neuroprotective. Using a well characterized in vitro model of brain cell trauma, we examined the potential role of exogenous S100B in preventing delayed neuronal injury. Neuronal plus glial cultures were grown on a deformable Silastic membrane and then subjected to strain (stretch) injury produced by a 50 ms displacement of the membrane. We have previously shown that this injury causes an immediate, but transient, nuclear uptake of the fluorescent dye propidium iodide by astrocytes and a 24-48 h delayed uptake by neurons. Strain injury caused immediate release of S100-beta with further release by 24 and 48 h. Adding 10 or 100 nm S100B to injured cultures at 15 s, 6 h or 24 h after injury reduced delayed neuronal injury measured at 48 h. Exogenous S100B was present in the cultures through 48 h. These studies directly demonstrate the release and neuroprotective role of S100B after traumatic injury and that, unlike most receptor antagonists used for the treatment of trauma, S100B is neuroprotective when given at later, more therapeutically relevant time points. 相似文献
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In smooth muscle, Ca(2+) controls diverse activities including cell division, contraction and cell death. Of particular significance in enabling Ca(2+) to perform these multiple functions is the cell's ability to localize Ca(2+) signals to certain regions by creating high local concentrations of Ca(2+) (microdomains), which differ from the cytoplasmic average. Microdomains arise from Ca(2+) influx across the plasma membrane or release from the sarcoplasmic reticulum (SR) Ca(2+) store. A single Ca(2+) channel can create a microdomain of several micromolar near (approximately 200 nm) the channel. This concentration declines quickly with peak rates of several thousand micromolar per second when influx ends. The high [Ca(2+)] and the rapid rates of decline target Ca(2+) signals to effectors in the microdomain with rapid kinetics and enable the selective activation of cellular processes. Several elements within the cell combine to enable microdomains to develop. These include the brief open time of ion channels, localization of Ca(2+) by buffering, the clustering of ion channels to certain regions of the cell and the presence of membrane barriers, which restrict the free diffusion of Ca(2+). In this review, the generation of microdomains arising from Ca(2+) influx across the plasma membrane and the release of the ion from the SR Ca(2+) store will be discussed and the contribution of mitochondria and the Golgi apparatus as well as endogenous modulators (e.g. cADPR and channel binding proteins) will be considered. 相似文献
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Ca microdomains in smooth muscle 总被引:1,自引:0,他引:1
John G. McCarron Susan Chalmers Karen N. Bradley Debbi MacMillan Thomas C. Muir 《Cell calcium》2006,40(5-6):461
In smooth muscle, Ca2+ controls diverse activities including cell division, contraction and cell death. Of particular significance in enabling Ca2+ to perform these multiple functions is the cell's ability to localize Ca2+ signals to certain regions by creating high local concentrations of Ca2+ (microdomains), which differ from the cytoplasmic average. Microdomains arise from Ca2+ influx across the plasma membrane or release from the sarcoplasmic reticulum (SR) Ca2+ store. A single Ca2+ channel can create a microdomain of several micromolar near (200 nm) the channel. This concentration declines quickly with peak rates of several thousand micromolar per second when influx ends. The high [Ca2+] and the rapid rates of decline target Ca2+ signals to effectors in the microdomain with rapid kinetics and enable the selective activation of cellular processes. Several elements within the cell combine to enable microdomains to develop. These include the brief open time of ion channels, localization of Ca2+ by buffering, the clustering of ion channels to certain regions of the cell and the presence of membrane barriers, which restrict the free diffusion of Ca2+. In this review, the generation of microdomains arising from Ca2+ influx across the plasma membrane and the release of the ion from the SR Ca2+ store will be discussed and the contribution of mitochondria and the Golgi apparatus as well as endogenous modulators (e.g. cADPR and channel binding proteins) will be considered. 相似文献
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Abhishek Abhishek Sally Doherty Rose Maciewicz Kenneth Muir Weiya Zhang Michael Doherty 《Arthritis research & therapy》2012,14(5):1-5