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Co‐expression/co‐location of S100 proteins (S100B, S100A1 and S100A2) and protein kinase C (PKC‐β, ‐η and ‐ζ) in a rat model of cerebral basilar artery vasospasm

Object: The cellular events leading to cerebral vasospasm after subarachnoid haemorrhages (SAH) involve a number of members of the protein kinase C (PKC) family. However, whereas calcium is thought to play a number of major roles in the pathophysiology of SAH, a number of PKCs function independently of calcium. We recently emphasized the potential role of the calcium‐binding S100 proteins in a ‘double haemorrhage’ rat model of SAH‐induced vasospasm. A number of S100 proteins are known to interfere directly with PKC, or indirectly with PKC substrates. We therefore investigated whether specific S100 proteins and PKCs are co‐expressed/co‐located in a rat model of SAH‐induced vasospasm. Methods and Results: SAH‐induced vasospasm in rats (by means of a double cisternal injection of autologous blood from a rat femoral artery) distinctly modified the expression levels of calcium‐dependent PKC‐α and PKC‐β and calcium‐independent PKC‐η and PKC‐ζ in endothelial and smooth‐muscle cells. The RNA levels of these four PKC isotypes were determined by quantitative RT‐PCR. The present study reveals that, in endothelial cells, the S100B expression/location correlate well with those of PKC‐η, and those of S100A1 with PKC‐β. In smooth‐muscle cells S100A2 expression/location correlate with those of PKC‐η, and those of S100B with PKC‐ζ. Conclusion: The present data argue in favour of a joint action of the S100 protein network and the PKC signalling pathway during cerebral vasospasm.