Article

Annexin VII: an astroglial protein exhibiting a Ca2+-dependent subcellular distribution.

Institute of Biochemistry, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 52, 50931 Cologne, Germany.
Neuroreport (Impact Factor: 1.4). 06/2001; 12(6):1139-44. DOI: 10.1097/00001756-200105080-00018
Source: PubMed

ABSTRACT A fundamental issue in neuronal and glial cells is how intracellular rises in Ca2+ are coupled to signaling cascades and changes in subcellular morphology. We studied the expression and localization of annexin VII (synexin), a Ca(2+)-/GTP-dependent membrane fusion protein, in the human CNS. Here, we demonstrate the presence of two annexin VII isoforms (47 and 51 kDa) in human brain tissue as well as its exclusive expression in astroglial cells. An in vitro study of astrocyte-derived C6 rat glioblastoma cells expressing a GFP tagged annexin VII fusion protein demonstrates a sequential redistribution of the fusion protein in response to rising intracellular Ca2+ concentrations. Our findings indicate a role of annexin VII in the regulation of intracellular Ca(2+)-dependent processes in astroglial cells.

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This defect does not interfere with the viability of animals maintained under normal conditions. Here we examined the cardiovascular phenotype of the knock-out mouse and the heart function under stress. Heart weight and weight of the ventricles is normal in the annexin A7 mouse. Analysing electrocardiograms from annexin A7 deficient mice we observed a reduced PQ-time and QRS-complex-time and a bradycardia. This suggested a role for annexin A7 in electromechanical coupling, probably through Ca2+ homeostasis. At last, it should be noted that the induction of a cardial hypertrophy failed in our study. This appears to be due to the high sensitivity of the mouse strain SV129 to the applicated drugs.