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J Biol Chem, Vol. 273, Issue 21, 12746-12752, May 22, 1998
From the Department of Microbiology and Molecular Genetics,
University of California, Irvine, California 92717-4025
This study examined the signal transduction
pathways involved in thrombin-induced neuroprotection and compares
these results with those of a similar study of thrombin-induced
neuronal death. In thrombin-induced protection of astrocytes from
hypoglycemia, pretreatment of astrocytes with tyrosine or
serine/threonine kinase inhibitors, cytochalasin D, or exoenzyme C3, a
potent inhibitor of the small GTPase RhoA, attenuated thrombin-induced
protection. These same inhibitors were previously shown to block
thrombin-induced cell death, implying a similarity in the cell death
and cell-protective pathways. Biochemical assays determined that
thrombin increased available RhoA activity, although more slowly and to
a lesser extent than occurs in thrombin-induced cell death. A clear
difference in these pathways was revealed when a time course study of
thrombin-induced cell death indicated that unlike thrombin-induced
protection, cells must be exposed to thrombin for >16 h to
irreversibly enter the cell death pathway. Addition of lower doses of
thrombin every 24 h also induced cell death. These studies
indicate that exposure of cells to micromolar concentrations of
thrombin alone does not induce cell death, but the continued exposure
to thrombin is required. Thus the cell death and protective pathways
may share initial signaling proteins, but differences in the amplitude
as well as the duration of the signal may result in different final
pathways.
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