Plau/Plaur double-deficiency did not worsen lesion severity or vascular integrity after traumatic brain injury
Autor: | Jenni Kyyriäinen, Asla Pitkänen, Jesse Tapiala, Anssi Lipponen, Xavier Ekolle Ndode-Ekane |
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Rok vydání: | 2020 |
Předmět: |
Male
0301 basic medicine Pathology medicine.medical_specialty Angiogenesis Traumatic brain injury Neuroprotection Receptors Urokinase Plasminogen Activator Receptor Platelet-Derived Growth Factor beta Lesion 03 medical and health sciences 0302 clinical medicine Growth factor receptor Brain Injuries Traumatic medicine Animals Receptor Mice Knockout business.industry General Neuroscience Brain medicine.disease Urokinase receptor Disease Models Animal 030104 developmental biology medicine.anatomical_structure Blood-Brain Barrier Female Pericyte medicine.symptom business 030217 neurology & neurosurgery |
Zdroj: | Neuroscience Letters. 729:134935 |
ISSN: | 0304-3940 |
Popis: | Binding of urokinase-type plasminogen activator receptor (uPAR) to its ligand uPA or to its plasma membrane partner, platelet-derived growth factor receptor β (PDGFRβ), promotes neuroprotection, cell proliferation, and angiogenesis. Following injury, single deficiency in uPA or uPAR leads in increased tissue loss and compromised vascular remodeling. We hypothesized that double-deficiency of uPAR (Plaur) and uPA (Plau) would result in increased lesion area and poor vascular integrity after traumatic brain injury (TBI). TBI was induced by lateral fluid-percussion injury in Plau/Plaur double-knockout (dKO) and wild-type (Wt) mice. The cortical lesion area was quantified in unfolded cortical maps prepared from thionin-stained sections at 4 d or 30 d post-TBI. The density of PDGFRβ+ pericytes and blood vessels was calculated from immunostained sections. Blood-brain barrier leakage was analyzed using ImageJ® from IgG-immunostained sections. Genotype had no effect on the total area of the cortical lesion at 4 d or 30 d post-TBI (p 0.05) or its progression as the overall lesion area was comparable at 4 d and 30 d post-TBI in both genotypes (p 0.05). Subfield analysis, however, indicated that damage to the visual cortex at 4 d post-TBI in dKO-TBI mice was 53 % of that in Wt-TBI mice (p 0.05). Both genotypes had a higher density of PDGFRβ-positive pericytes at 4 d than at 30 d post-TBI (p 0.05), but no genotype effect was detected between these time-points (p 0.05). TBI-induced increase in the density of PDGFRβ+ blood vessels at the region adjacent to the lesion core was comparable in both genotypes (p 0.05). Genotype had no effect on TBI-induced IgG leakage into the perilesional cortical parenchyma (p 0.05). Contrary to our expectations, Plau/Plaur double-deficiency did not aggravate TBI-related structural outcome. |
Databáze: | OpenAIRE |
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