PMID- 25445237
OWN - NLM
STAT- MEDLINE
DCOM- 20150804
LR  - 20211203
IS  - 1872-6844 (Electronic)
IS  - 0920-1211 (Linking)
VI  - 108
IP  - 10
DP  - 2014 Dec
TI  - Role of TGF-beta signaling pathway on Tenascin C protein upregulation in a 
      pilocarpine seizure model.
PG  - 1694-704
LID - S0920-1211(14)00252-6 [pii]
LID - 10.1016/j.eplepsyres.2014.09.019 [doi]
AB  - 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-beta 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-beta1 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-beta1 and the critical 
      downstream transduction effector phospho-Smad2/3 throughout the chronic exposure. 
      Interestingly, animals injected with SB-431542, a TGF-beta-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-beta 
      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.
CI  - Copyright (c) 2014 Elsevier B.V. All rights reserved.
FAU - Mercado-Gomez, Octavio
AU  - Mercado-Gomez O
AD  - Departamento de Fisiologia, Facultad de Medicina, Universidad Nacional Autonoma 
      de Mexico, 04510 Mexico, DF, Mexico.
FAU - Landgrave-Gomez, Jorge
AU  - Landgrave-Gomez J
AD  - Departamento de Fisiologia, Facultad de Medicina, Universidad Nacional Autonoma 
      de Mexico, 04510 Mexico, DF, Mexico.
FAU - Arriaga-Avila, Virginia
AU  - Arriaga-Avila V
AD  - Departamento de Fisiologia, Facultad de Medicina, Universidad Nacional Autonoma 
      de Mexico, 04510 Mexico, DF, Mexico.
FAU - Nebreda-Corona, Adriana
AU  - Nebreda-Corona A
AD  - Departamento de Fisiologia, Facultad de Medicina, Universidad Nacional Autonoma 
      de Mexico, 04510 Mexico, DF, Mexico.
FAU - Guevara-Guzman, Rosalinda
AU  - Guevara-Guzman R
AD  - Departamento de Fisiologia, Facultad de Medicina, Universidad Nacional Autonoma 
      de Mexico, 04510 Mexico, DF, Mexico. Electronic address: rguevara@unam.mx.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141019
PL  - Netherlands
TA  - Epilepsy Res
JT  - Epilepsy research
JID - 8703089
RN  - 0 (4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide)
RN  - 0 (Benzamides)
RN  - 0 (Central Nervous System Agents)
RN  - 0 (Dioxoles)
RN  - 0 (Receptors, Transforming Growth Factor beta)
RN  - 0 (Smad2 Protein)
RN  - 0 (Smad2 protein, rat)
RN  - 0 (Smad3 Protein)
RN  - 0 (Smad3 protein, rat)
RN  - 0 (Tenascin)
RN  - 0 (Transforming Growth Factor beta)
RN  - 01MI4Q9DI3 (Pilocarpine)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 2.7.11.30 (Receptor, Transforming Growth Factor-beta Type I)
RN  - EC 2.7.11.30 (Tgfbr1 protein, rat)
SB  - IM
MH  - Animals
MH  - Benzamides/pharmacology
MH  - Cell Nucleus/drug effects/metabolism
MH  - Central Nervous System Agents/pharmacology
MH  - Cytoplasm/drug effects/metabolism
MH  - Dioxoles/pharmacology
MH  - Disease Models, Animal
MH  - Hippocampus/drug effects/*metabolism
MH  - Male
MH  - Phosphorylation
MH  - Pilocarpine
MH  - Protein Serine-Threonine Kinases/*metabolism
MH  - Rats, Wistar
MH  - Receptor, Transforming Growth Factor-beta Type I
MH  - Receptors, Transforming Growth Factor beta/*metabolism
MH  - Seizures/*metabolism
MH  - Signal Transduction/drug effects
MH  - Smad2 Protein/metabolism
MH  - Smad3 Protein/metabolism
MH  - Tenascin/*metabolism
MH  - Transforming Growth Factor beta/antagonists & inhibitors/*metabolism
MH  - Up-Regulation/drug effects
OTO - NOTNLM
OT  - Hippocampus
OT  - Phospho-Smad2/3
OT  - Pilocarpine
OT  - Status epilepticus
OT  - Tenascin C
OT  - Transforming growth factor beta
EDAT- 2014/12/03 06:00
MHDA- 2015/08/05 06:00
CRDT- 2014/12/03 06:00
PHST- 2014/04/27 00:00 [received]
PHST- 2014/08/29 00:00 [revised]
PHST- 2014/09/21 00:00 [accepted]
PHST- 2014/12/03 06:00 [entrez]
PHST- 2014/12/03 06:00 [pubmed]
PHST- 2015/08/05 06:00 [medline]
AID - S0920-1211(14)00252-6 [pii]
AID - 10.1016/j.eplepsyres.2014.09.019 [doi]
PST - ppublish
SO  - Epilepsy Res. 2014 Dec;108(10):1694-704. doi: 10.1016/j.eplepsyres.2014.09.019. 
      Epub 2014 Oct 19.