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What is the role of PDGFRβ and uPAR proteins in brain injury pathology?

  • Health and well-being

The doctoral thesis of Jenni Kyyriäinen, MSc, demonstrates how cells expressing PDGFRβ protein accumulate in injured brain areas. The results shed light on the pathology mechanisms occurring after status epilepticus and traumatic brain injury. The public examination will be held online on 20th November 2020 starting at 12 noon.

Brain injury is followed by neuroplasticity

The extracellular matrix (ECM) contributes to post-injury tissue remodeling by initiating proliferation and migration of the cells needed for angiogenesis and scar formation. One complex of the ECM is the urokinase-type plasminogen activator receptor (uPAR) interactome, which includes its primary ligand, the urokinase-type plasminogen activator (uPA), and co-receptors such as the platelet-derived growth factor receptor (PDGFR) β. The expression of the components of the uPAR interactome increases after injury, suggesting engagement in tissue and vascular plasticity.

The aim of Kyyriäinen’s thesis was to investigate the role of the uPAR and the PDGFRβ in tissue and vascular pathology and plasticity after brain injury. First, the researchers characterized a double-knockout mouse model deficient both in Plau, the gene encoding uPA, and in Plaur, the gene encoding uPAR. In the characterization, they used a behavioral test battery and a pentylenetetrazol (PTZ) test under video-EEG, wherein the development of epilepsy phenotype was monitored. Next, the expression pattern of the PDGFRβ was demonstrated in wild-type mice after status epilepticus as well as in rats and wild-type and double-knockout mice after traumatic brain injury (TBI), by using immunohistochemistry and stereology.

In double-knockout mice, the researchers demonstrated increased susceptibility to seizures after PTZ administration, seizures unaccompanied by change in the number of perineuronal nets, a structure surrounding GABAergic neurons. In rats and both double-knockout and wild-type mice, TBI induced the accumulation of PDGFRβ+ pericytes and glial cells at the lesion site, suggesting that the migration of these cells is not exclusively uPAR-mediated. Similar clustering of PDGFRβ+ cells was also seen after status epilepticus in wild-type mice. Finally, Plau/Plaur deficiency did not increase post-TBI blood-brain barrier damage.

The doctoral dissertation of Jenni Kyyriäinen, MSc, entitled The role of the platelet-derived growth factor receptor β and the urokinase-type plasminogen activator receptor in brain injury pathology, will be examined at the Faculty of Health Sciences. The Opponent in the public examination will be Associate Professor Hana Kubová of the Czech Academy of Sciences, and the Custos will be Professor Asla Pitkänen of the University of Eastern Finland. The public examination will be held in English.

Photo available for download at

Dissertation online:

Kyyriäinen, Jenni. The role of the platelet-derived growth factor receptor and the urokinase-type plasminogen activator receptor in brain injury pathology