On the endothelial cell ISOC
2003; Elsevier BV; Volume: 33; Issue: 5-6 Linguagem: Inglês
10.1016/s0143-4160(03)00046-0
ISSN1532-1991
AutoresDonna L. Cioffi, Songwei Wu, Troy Stevens,
Tópico(s)Neurobiology and Insect Physiology Research
ResumoCa2+ store depletion activates both Ca2+ selective and non-selective currents in endothelial cells. Recently, considerable progress has been made in understanding the molecular make-up and regulation of an endothelial cell thapsigargin-activated Ca2+ selective current, ISOC. Indeed, ISOC is a relatively small inward Ca2+ current that exhibits an approximate +40 mV reversal potential and is strongly inwardly rectifying. This current is sensitive to organization of the actin-based cytoskeleton. Transient receptor potential (TRP) proteins 1 and 4 (TRPC1 and TRPC4, respectively) each contribute to the molecular basis of ISOC, although it is TRPC4 that appears to be tethered to the cytoskeleton through a dynamic interaction with protein 4.1. Activation of ISOC requires association between protein 4.1 and the actin-based cytoskeleton (mediated through spectrin), suggesting protein 4.1 mediates the physical communication between Ca2+ store depletion and channel activation. Thus, at present findings indicate a TRPC4–protein 4.1 physical linkage regulates ISOC activation following Ca2+ store depletion.
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