PMID- 24481545
OWN - NLM
STAT- MEDLINE
DCOM- 20141106
LR  - 20211021
IS  - 1868-601X (Electronic)
IS  - 1868-4483 (Linking)
VI  - 5
IP  - 2
DP  - 2014 Apr
TI  - Tenascin-C causes neuronal apoptosis after subarachnoid hemorrhage in rats.
PG  - 238-47
LID - 10.1007/s12975-014-0333-2 [doi]
AB  - The role of tenascin-C (TNC), a matricellular protein, in brain injury is 
      unknown. The aim of this study was to examine if TNC causes neuronal apoptosis 
      after subarachnoid hemorrhage (SAH), a deadly cerebrovascular disorder, using 
      imatinib mesylate (a selective inhibitor of platelet-derived growth factor 
      receptor [PDGFR] that is reported to suppress TNC induction) and recombinant TNC. 
      SAH by endovascular perforation caused caspase-dependent neuronal apoptosis in 
      the cerebral cortex irrespective of cerebral vasospasm development at 24 and 72 h 
      post-SAH, associated with PDGFR activation, mitogen-activated protein kinases 
      (MAPKs) activation, and TNC induction in rats. PDGFR inactivation by an 
      intraperitoneal injection of imatinib mesylate prevented neuronal apoptosis, as 
      well as MAPKs activation and TNC induction in the cerebral cortex at 24 h. A 
      cisternal injection of recombinant TNC reactivated MAPKs and abolished 
      anti-apoptotic effects of imatinib mesylate. The TNC injection also induced TNC 
      itself in SAH brain, which may internally augment neuronal apoptosis after SAH. 
      These findings suggest that TNC upregulation by PDGFR activation causes neuronal 
      apoptosis via MAPK activation, and that the positive feedback mechanisms may 
      exist to augment neuronal apoptosis after SAH. TNC-induced neuronal apoptosis 
      would be a new target to improve outcome after SAH.
FAU - Shiba, Masato
AU  - Shiba M
AD  - Department of Neurosurgery, Mie University Graduate School of Medicine, 2-174 
      Edobashi, Tsu, Mie, 514-8507, Japan.
FAU - Fujimoto, Masashi
AU  - Fujimoto M
FAU - Imanaka-Yoshida, Kyoko
AU  - Imanaka-Yoshida K
FAU - Yoshida, Toshimichi
AU  - Yoshida T
FAU - Taki, Waro
AU  - Taki W
FAU - Suzuki, Hidenori
AU  - Suzuki H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140201
PL  - United States
TA  - Transl Stroke Res
JT  - Translational stroke research
JID - 101517297
RN  - 0 (Benzamides)
RN  - 0 (Piperazines)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 0 (Pyrimidines)
RN  - 0 (Tenascin)
RN  - 8A1O1M485B (Imatinib Mesylate)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects/*physiology
MH  - Benzamides/pharmacology
MH  - Disease Models, Animal
MH  - Imatinib Mesylate
MH  - Neurons/drug effects/*metabolism/pathology
MH  - Piperazines/pharmacology
MH  - Protein Kinase Inhibitors/pharmacology
MH  - Pyrimidines/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Subarachnoid Hemorrhage/*metabolism/pathology
MH  - Tenascin/*metabolism
MH  - Vasospasm, Intracranial/*metabolism/pathology
EDAT- 2014/02/01 06:00
MHDA- 2014/11/07 06:00
CRDT- 2014/02/01 06:00
PHST- 2013/11/02 00:00 [received]
PHST- 2014/01/16 00:00 [accepted]
PHST- 2014/01/15 00:00 [revised]
PHST- 2014/02/01 06:00 [entrez]
PHST- 2014/02/01 06:00 [pubmed]
PHST- 2014/11/07 06:00 [medline]
AID - 10.1007/s12975-014-0333-2 [doi]
PST - ppublish
SO  - Transl Stroke Res. 2014 Apr;5(2):238-47. doi: 10.1007/s12975-014-0333-2. Epub 
      2014 Feb 1.