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. [ABSTRACT FROM AUTHOR]