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. Author manuscript; available in PMC: 2012 Nov 7.
Published in final edited form as: Trends Neurosci. 2011 Feb 25;34(4):198–209. doi: 10.1016/j.tins.2011.01.005

Figure 2. Control of ischemic injury to the neurovascular unit by APC and/or its cell-signaling analogs.

Figure 2

APC protects the BBB integrity and ameliorates post-ischemic BBB breakdown thus preventing secondary neuronal damage mediated by entry of several blood-derived neurotoxic and vasculotoxic molecules. It crosses an intact BBB via EPCR-dependent transport to reach its neuronal targets in brain and expresses its direct neuronal protective activity to prevent neuronal damage. APC also expresses anti-inflammatory activities by blocking early post-ischemic infiltration of brain by neutrophils. It also suppresses microglia activation. The key membrane signaling receptor mediating beneficial effects of APC on different cell types within the neurovascular unit is PAR1, as illustrated in Figure 3.