Partner Profile

Center of Cerebrovascular Plasticity


Areas of Expertise

In recent years, we have, in a series of studies, revealed a novel aspect of the cerebrovascular pathology in focal and global ischemic stroke and SAH; it is associated with expressional upregulation of vasoconstrictor receptors and inflammation mediators in cerebral arteries. The expression of contractile endothelin B (ETB) and 5-hydroxytryptamine 1B (5-HT1B) receptors in cerebrovascular smooth muscle cells is increased, not only in the large cerebral arteries, but also in intracerebral microvessels. The upregulation process is mediated by intracellular signalling via the mitogen-activated protein kinase (MEK1/2) – extracellular regulated kinase 1/2 (ERK1/2) pathway while p38 and JNK increase their expression much later.

We hypothesise that it is the drop in brain blood flow and the decrease in wall tension (reduced shear stress) experienced by cerebral arteries in acute stroke that is a key triggering event, which, via early MEK-ERK1/2 activation in cerebral arteries, initiates the process of cerebrovascular vasoconstrictor receptor upregulation contributing to the development of late cerebral ischemia and somewhat later initiating the upregulation of inflammation mediators. We aim to develop specific inhibitors that can interact with this process and thereby reduce the tissue damage after a stroke and invite interested scientists and companies to collaborate.

Recent Publications

Research Interests
  • Understanding of intracellular signalling networks and transcription factors activated in the cerebral vessel walls in different forms of stroke
  • How the individual components of receptors, inflammation and blood-brain barrier proteins are related in stroke
  • The way in which the signalling and receptors relate to the neurovascular unit and network in stroke
  • Whether the same mechanisms are in play in human stroke; and
  • If early blockade of MEK/ERK signalling affects the short-term outcome after a stroke will
    this involve angiogenesis and neurogenesis in the long-term outcome?