Compounds > 4-(5-benzo(1-3)dioxol-5-yl-4-pyridin-2-yl-1h-imidazol-2-yl)benzamide

4-(5-benzo(1-3)dioxol-5-yl-4-pyridin-2-yl-1h-imidazol-2-yl)benzamide and Seizures

4-(5-benzo(1-3)dioxol-5-yl-4-pyridin-2-yl-1h-imidazol-2-yl)benzamide has been researched along with Seizures* in 1 studies

Other Studies

1 other study(ies) available for 4-(5-benzo(1-3)dioxol-5-yl-4-pyridin-2-yl-1h-imidazol-2-yl)benzamide and Seizures

Article	Year
Role of TGF-β signaling pathway on Tenascin C protein upregulation in a pilocarpine seizure model. Epilepsy research, 2014, Volume: 108, Issue:10 Seizures have been shown to upregulate the expression of numerous extracellular matrix molecules. Tenascin C (TNC) is an extracellular matrix protein involved in several physiological roles and in pathological conditions. Though TNC upregulation has been described after excitotoxins injection, to date there is no research work on the signal transduction pathway(s) participating in TNC protein overproduction. The aim of this study was to evaluate the role of TGF-β signaling pathway on TNC upregulation. In this study, we used male rats, which were injected with saline or pilocarpine to induce status epilepticus (SE) and killed 24h, 3 and 7 days after pilocarpine administration. For evaluating biochemical changes, we measured protein content of TNC, TGF-β1 and phospho-Smad2/3 for localization of TNC in coronal brain hippocampus at 24h, 3 and 7 days after pilocarpine-caused SE. We found a significant increase of TNC protein content in hippocampal homogenates after 1, 3, and 7 days of pilocarpine-caused SE, together with an enhancement of TNC immunoreactivity in several hippocampal layers and the dentate gyrus field where more dramatic changes occurred. We also observed a significant enhancement of protein content of both the TGF-β1 and the critical downstream transduction effector phospho-Smad2/3 throughout the chronic exposure. Interestingly, animals injected with SB-431542, a TGF-β-type I receptor inhibitor, decreased TNC content in cytosolic fraction and diminished phospho-Smad2/3 content in both cytoplasmic and nuclear fraction compared with pilocarpine vehicle-injected. These findings suggest the participation of TGF-β signaling pathway on upregulation of TNC which in turn support the idea that misregulation of this signaling pathway produces changes that may contribute to disease. Topics: Animals; Benzamides; Cell Nucleus; Central Nervous System Agents; Cytoplasm; Dioxoles; Disease Models, Animal; Hippocampus; Male; Phosphorylation; Pilocarpine; Protein Serine-Threonine Kinases; Rats, Wistar; Receptor, Transforming Growth Factor-beta Type I; Receptors, Transforming Growth Factor beta; Seizures; Signal Transduction; Smad2 Protein; Smad3 Protein; Tenascin; Transforming Growth Factor beta; Up-Regulation	2014

Article

Year

Role of TGF-β signaling pathway on Tenascin C protein upregulation in a pilocarpine seizure model.

Epilepsy research, 2014, Volume: 108, Issue:10

Seizures have been shown to upregulate the expression of numerous extracellular matrix molecules. Tenascin C (TNC) is an extracellular matrix protein involved in several physiological roles and in pathological conditions. Though TNC upregulation has been described after excitotoxins injection, to date there is no research work on the signal transduction pathway(s) participating in TNC protein overproduction. The aim of this study was to evaluate the role of TGF-β signaling pathway on TNC upregulation. In this study, we used male rats, which were injected with saline or pilocarpine to induce status epilepticus (SE) and killed 24h, 3 and 7 days after pilocarpine administration. For evaluating biochemical changes, we measured protein content of TNC, TGF-β1 and phospho-Smad2/3 for localization of TNC in coronal brain hippocampus at 24h, 3 and 7 days after pilocarpine-caused SE. We found a significant increase of TNC protein content in hippocampal homogenates after 1, 3, and 7 days of pilocarpine-caused SE, together with an enhancement of TNC immunoreactivity in several hippocampal layers and the dentate gyrus field where more dramatic changes occurred. We also observed a significant enhancement of protein content of both the TGF-β1 and the critical downstream transduction effector phospho-Smad2/3 throughout the chronic exposure. Interestingly, animals injected with SB-431542, a TGF-β-type I receptor inhibitor, decreased TNC content in cytosolic fraction and diminished phospho-Smad2/3 content in both cytoplasmic and nuclear fraction compared with pilocarpine vehicle-injected. These findings suggest the participation of TGF-β signaling pathway on upregulation of TNC which in turn support the idea that misregulation of this signaling pathway produces changes that may contribute to disease.

Topics: Animals; Benzamides; Cell Nucleus; Central Nervous System Agents; Cytoplasm; Dioxoles; Disease Models, Animal; Hippocampus; Male; Phosphorylation; Pilocarpine; Protein Serine-Threonine Kinases; Rats, Wistar; Receptor, Transforming Growth Factor-beta Type I; Receptors, Transforming Growth Factor beta; Seizures; Signal Transduction; Smad2 Protein; Smad3 Protein; Tenascin; Transforming Growth Factor beta; Up-Regulation

2014