Astrocytic thrombin-evoked VEGF release is dependent on p44/42 MAPKs and PAR1.

Intracerebral haemorrhage (ICH) often causes severe neurological deficits in survived patients, although its underlying mechanisms remain elusive. A common feature of ICH is the accumulation of thrombin around the lesion site. Previous studies showed that thrombin promotes VEGF release and angiogenesis at a late stage post ICH [1]. In current study, we explored the source for thrombin-induced VEGF release by adding thrombin or its receptor agonist peptide to the neuronal or astrocytic primarily cultures. We identified that astrocytes specifically respond to thrombin by up-regulating and releasing VEGF. Furthermore, such release is dependent on p44/42 MAPKs and PAR1, a thrombin specific receptor. Our study therefore helps clarifying the underlying mechanisms of thrombin-induced VEGF release in ICH, which will further provide novel insights into the designing principles for treating ICH and traumatic brain injuries.

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