Co-expression/co-location of S100 proteins (S100B, S100A1 and S100A2) and protein kinase C (PKC-beta, -eta and -zeta) in a rat model of cerebral basilar artery vasospasm.
OBJECTIVE
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.


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-alpha and PKC-beta and calcium-independent PKC-eta and PKC-zeta 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-eta, and those of S100A1 with PKC-beta. In smooth-muscle cells S100A2 expression/location correlate with those of PKC-eta, and those of S100B with PKC-zeta.


CONCLUSIONS
The present data argue in favour of a joint action of the S100 protein network and the PKC signalling pathway during cerebral vasospasm.
Lefranc
F
F
Department of Neurosurgery, Erasmus University Hospital, Belgium.
Decaestecker
C
C
Brotchi
J
J
Heizmann
C W
CW
Dewitte
O
O
Kiss
R
R
Mijatovic
T
T
D000818:Animals; D001488:Basilar Artery / Q000502:physiology; D015153:Blotting, Western; D002135:Calcium-Binding Proteins / Q000235:genetics* / Q000378:metabolism; D002630:Chemotactic Factors / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D009414:Nerve Growth Factors / Q000235:genetics* / Q000378:metabolism; D011493:Protein Kinase C / Q000235:genetics* / Q000378:metabolism; D064546:Protein Kinase C beta; D051571:Protein Kinase C-alpha / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000235:genetics* / Q000378:metabolism; D013345:Subarachnoid Hemorrhage / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D020301:Vasospasm, Intracranial / Q000235:genetics* / Q000378:metabolism* / Q000503:physiopathology; D014715:Vertebrobasilar Insufficiency / Q000235:genetics* / Q000378:metabolism* / Q000503:physiopathology; D000099221:Protein Kinase C zeta
D002135:Calcium-Binding Proteins; D002630:Chemotactic Factors; D009414:Nerve Growth Factors; D011493:Protein Kinase C; D064546:Protein Kinase C beta; D051571:Protein Kinase C-alpha; D012333:RNA, Messenger; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; D000099221:Protein Kinase C zeta; C110294:S100A1 protein; C483336:S100A2 protein, rat; C579158:S100b protein, rat; C081975:protein kinase C eta