Epileptogenesis after traumatic brain injury in Plau-deficient mice

Decreased levels of active uPA and KLK8 assessed by [111In]MICA‐401 binding correlate with the seizure burden in an animal model of temporal lobe epilepsy

“…A pronounced decrease in uPA expression following KASE might result in the failure to initiate the appropriate repair mechanisms, leading to a worse behavioral phenotype. However, uPA deficiency did not have an effect on epilepsy phenotype following KASE or epileptogenesis following CCI injury in mice . On the other hand, deficiency of KLK8 did result in increased seizure susceptibility to kainic acid .…”

Deficiency of urokinase-type plasminogen activator and its receptor affects social behavior and increases seizure susceptibility

“…The expression of uPAR and uPA is normally low in neurons, microglia, astrocytes, and vascular cells, but becomes robustly upregulated after epileptogenic brain injury in both experimental models (Lahtinen et al, 2006(Lahtinen et al, , 2009 and humans (Liu et al, 2010;Iyer et al, 2010). Mice with Plau or Plaur deficiency have impaired post-injury recovery (Morales et al, 2006;Lahtinen et al, 2010;Ndode-Ekane and Pitkanen 2013;Rantala et al, 2015; Bolkvadze et al, 2015Bolkvadze et al, , 2016. Moreover, the brain tissue of patients with drug-refractory epilepsy exhibits increased uPA and/or uPAR expression (Liu et al, 2010;Iyer et al, 2010).…”

“…We previously characterized the neurophenotype of Plau-and Plaur-deficient mice and their response to epileptogenic brain injury (Lahtinen et al, 2010;Ndode-Ekane and Pitkanen 2013;Rantala et al, 2015;Bolkvadze et al, 2015Bolkvadze et al, , 2016. To further elucidate the involvement of individual components of the uPAR interactome in normal behavior and the response to stimuli, we performed extensive behavioral testing of double knockout mice (dKO) lacking both Plau and Plaur in exploratory activity, social interaction, and anxiety, as well as learning and memory tests.…”

Effect of recombinant human erythropoietin expressions of apoptosis genes in rats following traumatic brain injury

“…In addition, it is reported that over 5 % of patients with moderate injury, and 16 % of patients with severe injury would develop posttraumatic epilepsy [2,3]. The mechanisms underlying secondary brain damage following TBI are complex and involve two main stages: traumatic cerebral edema and delayed neuronal damage [1][2][3]. Delayed neuronal damage leads to irreversible necrosis or apoptosis of neurons, which could affect the long-term prognosis and quality of life in patients [1,2,4,5].…”

“…The mechanisms underlying secondary brain damage following TBI are complex and involve two main stages: traumatic cerebral edema and delayed neuronal damage [1][2][3]. Delayed neuronal damage leads to irreversible necrosis or apoptosis of neurons, which could affect the long-term prognosis and quality of life in patients [1,2,4,5]. It is known that NF-kappa B (NF-κB) can result in neuronal damage by apoptosis.…”