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Projects - Protease-activated receptors (PARs) - Leibniz Institute for Neurobiology, Magdeburg
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 Protease-activated receptors (PARs)

Principle investigator: Monika Riek-Burchardt

We know for several years, that thrombin is not only a key enzyme in the coagulation cascade. Thrombin activates protease-activated receptors (PARs), which are also present in the brain. This activation mechanism is unique in that it involves the proteolytic unmasking of an amino-terminal receptor sequence, which acts as a tethered ligand. The function of thrombin/PARs in the CNS, especially in ischemic and inflammatory events is not clear. Now we could show, in contrast to the exclusively neuronal staining in the brain parenchyma of naïve animals, PAR1 and PAR3 occurred in addition on microglial cells in the penumbra after focal ischemia. Additionally, we demonstrated enhanced immunohistochemical PAR4 signals at the border zone and within the infarct area (Henrich-Noack et al., 2006a). Beside these interesting results of PAR expression, thrombin represents a remarkably role in the signal cascade after ischemia. We found extremly different thrombin-induced effects after ischemic insults: in different models of ischemia the thrombin application resulted as well as in a neuroprotection and in an extension of the damage (Striggow et al. 2000, Henrich-Noack et al 2006b). Using the same model of ischemia and changing the application scheme, we also received opposite effects. Like these thrombin effects the microglia activation during ischemia is a mixed blessing, we also suppose a correlation between the selective post-ischemic activation of microglia and the opposite thrombin action after ischemia.

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