PMID- 28244007
OWN - NLM
STAT- MEDLINE
DCOM- 20190523
LR  - 20210222
IS  - 1559-1182 (Electronic)
IS  - 0893-7648 (Linking)
VI  - 55
IP  - 3
DP  - 2018 Mar
TI  - Effects of Tenascin-C Knockout on Cerebral Vasospasm After Experimental 
      Subarachnoid Hemorrhage in Mice.
PG  - 1951-1958
LID - 10.1007/s12035-017-0466-x [doi]
AB  - A matricellular protein tenascin-C (TNC) has been suggested to play a role in the 
      pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH), but the 
      direct evidence remains lacking. In this study, we examined effects of TNC 
      knockout (TNKO) on cerebral vasospasm after experimental SAH in mice. C57BL/6 
      wild-type (WT) or TNKO mice were subjected to SAH by endovascular puncture. Ten 
      WT and ten TNKO mice were randomized to WT sham (n = 4), TNKO sham (n = 4), WT 
      SAH (n = 6), and TNKO SAH (n = 6) groups. In addition to neurobehavioral 
      impairments and severity of SAH, cerebral vasospasm was assessed by morphometric 
      measurements of the left internal carotid artery (ICA). Infiltration of 
      inflammatory cells in the subarachnoid periarterial space was also assessed, and 
      expressions of TNC and mitogen-activated protein kinases (MAPKs) in the ICA were 
      immunohistochemically evaluated at 24 h post-surgery. TNC was induced in the 
      smooth muscle cell layers and the adventitia in the spastic ICAs as well as the 
      periarterial inflammatory cells in WT SAH mice. Compared with WT SAH mice, TNKO 
      SAH mice showed better neurological scores and less severe cerebral vasospasm, as 
      well as fewer inflammatory cell infiltration in the periarterial space. Post-SAH 
      activation of MAPKs in the smooth muscle cell layers of the ICAs was also 
      prevented in TNKO SAH mice. The findings in the present study suggest that TNC 
      causes the development of cerebral vasospasm via pro-inflammatory effects and 
      activation of MAPKs.
FAU - Fujimoto, Masashi
AU  - Fujimoto M
AD  - Department of Neurosurgery, Mie University Graduate School of Medicine, 2-174 
      Edobashi, Tsu, Mie, 514-8507, Japan.
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 - Kawakita, Fumihiro
AU  - Kawakita F
AD  - Department of Neurosurgery, Mie University Graduate School of Medicine, 2-174 
      Edobashi, Tsu, Mie, 514-8507, Japan.
FAU - Liu, Lei
AU  - Liu L
AD  - Department of Neurosurgery, Mie University Graduate School of Medicine, 2-174 
      Edobashi, Tsu, Mie, 514-8507, Japan.
FAU - Shimojo, Naoshi
AU  - Shimojo N
AD  - Department of Pathology and Matrix Biology, Mie University Graduate School of 
      Medicine, 2-174 Edobashi, Tsu, Mie, 514-8507, Japan.
FAU - Imanaka-Yoshida, Kyoko
AU  - Imanaka-Yoshida K
AD  - Department of Pathology and Matrix Biology, Mie University Graduate School of 
      Medicine, 2-174 Edobashi, Tsu, Mie, 514-8507, Japan.
AD  - Research Center for Matrix Biology, Mie University Graduate School of Medicine, 
      2-174 Edobashi, Tsu, Mie, 514-8507, Japan.
FAU - Yoshida, Toshimichi
AU  - Yoshida T
AD  - Department of Pathology and Matrix Biology, Mie University Graduate School of 
      Medicine, 2-174 Edobashi, Tsu, Mie, 514-8507, Japan.
AD  - Research Center for Matrix Biology, Mie University Graduate School of Medicine, 
      2-174 Edobashi, Tsu, Mie, 514-8507, Japan.
FAU - Suzuki, Hidenori
AU  - Suzuki H
AUID- ORCID: 0000-0002-8555-5448
AD  - Department of Neurosurgery, Mie University Graduate School of Medicine, 2-174 
      Edobashi, Tsu, Mie, 514-8507, Japan. suzuki02@clin.medic.mie-u.ac.jp.
AD  - Research Center for Matrix Biology, Mie University Graduate School of Medicine, 
      2-174 Edobashi, Tsu, Mie, 514-8507, Japan. suzuki02@clin.medic.mie-u.ac.jp.
LA  - eng
GR  - 15K19962/Japan Society for the Promotion of Science/International
GR  - N/A/Mie Medical Research Foundation/International
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20170227
PL  - United States
TA  - Mol Neurobiol
JT  - Molecular neurobiology
JID - 8900963
RN  - 0 (Tenascin)
SB  - IM
MH  - Animals
MH  - Female
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Subarachnoid Hemorrhage/genetics/*metabolism
MH  - Tenascin/*deficiency/genetics
MH  - Vasospasm, Intracranial/genetics/*metabolism/*prevention & control
OTO - NOTNLM
OT  - Cerebral vasospasm
OT  - Mitogen-activated protein kinase
OT  - Subarachnoid hemorrhage
OT  - Tenascin-C
EDAT- 2017/03/01 06:00
MHDA- 2019/05/24 06:00
CRDT- 2017/03/01 06:00
PHST- 2016/12/31 00:00 [received]
PHST- 2017/02/20 00:00 [accepted]
PHST- 2017/03/01 06:00 [pubmed]
PHST- 2019/05/24 06:00 [medline]
PHST- 2017/03/01 06:00 [entrez]
AID - 10.1007/s12035-017-0466-x [pii]
AID - 10.1007/s12035-017-0466-x [doi]
PST - ppublish
SO  - Mol Neurobiol. 2018 Mar;55(3):1951-1958. doi: 10.1007/s12035-017-0466-x. Epub 
      2017 Feb 27.