Extracellular matrix protein SC1/hevin in the hippocampus following pilocarpine‐induced status epilepticus

Abstract

Pilocarpine‐induced status epilepticus (SE) mimics many features of temporal lobe epilepsy and is a useful model to study neural changes that result from prolonged seizure activity. In this study, distribution of the anti‐adhesive extracellular matrix protein SC1 was examined in the rat hippocampus following SE. Western blotting showed decreased levels of SC1 protein in the week following SE. Immunohistochemistry demonstrated that the decrease in overall SC1 protein levels was reflected by a reduction of SC1 signal in granule cells of the dentate gyrus. Interestingly, levels of SC1 protein in neurons of the seizure‐resistant CA2 sector of the hippocampus did not change throughout the seizure time course. However, at 1 day post‐SE, a subset of neurons of the hippocampal CA1, CA3, and hilar regions, which are noted for extensive neuronal degeneration after SE, exhibited a transient increase in SC1 signal. Neurons exhibiting enhanced SC1 signal were not detected at 7 days post‐SE. The cellular stress response was also examined. A prominent induction of heat‐shock protein (Hsp70) and Hsp27 was detected following SE, while levels of constitutively expressed Hsp40, Hsp90, Hsp110, and Hsc70 showed little change at the time points examined. The subset of neurons that demonstrated a transient increase in SC1 colocalized with the cellular stress marker Hsp70, the degeneration marker Fluoro‐Jade B, and the neuron activity marker activity‐regulated cytoskeleton‐associated protein (Arc). Taken together, these findings suggest that SC1 may be a component of the ‘matrix response’ involved in remodeling events associated with neuronal degeneration following neural injury.

Distribution and Time-Course of 4-Hydroxynonenal, Heat Shock Protein 110/105 Family Members and Cyclooxygenase-2 Expression in the Hippocampus of Rat During Trimethyltin-Induced Neurodegeneration

“…Interestingly, a similar dissociation in the behaviour of HSP 110/105 and HSP 70 protein families has also been reported in the model of pilocarpine-induced status epilepticus [55].…”

Integrins as receptor targets for neurological disorders

“…A transient increase in SC1 co-localization with the cellular stress marker Hsp70, the degeneration marker Fluoro-Jade B, and the neuron activity marker activity-regulated CSK-associated protein are also shown in neurons of the hippocampal CA1, CA3, and hilar regions after status epilepticus. The levels of SC1 protein in neurons of the hippocampal seizure-resistant CA2 region do not change throughout the seizure (Lively & Brown, 2008). …”

Identification of QTLs Involved in the Development of Amygdala Kindling in the Rat

“…Several sources in the literature have investigated genes that might be related to the kindling rate. In the Agkr1 locus, the genes Polo-like kinase 2 ( Plk2 ), heat shock protein-27 ( Hspb3 ), and integrins ( Itga1 , Itga2 ) [3, 7, 18] are upregulated in epileptic animals. In the Agkr2 locus, potassium voltage-gated channel beta member 1 ( Kcnab1 ), which is associated with idiopathic epilepsy [17], is upregulated.…”