View : 60 Download: 0

Extracellular signal-regulated kinase1/2-dependent changes in tight junctions after ischemic preconditioning contributes to tolerance induction after ischemic stroke

Title
Extracellular signal-regulated kinase1/2-dependent changes in tight junctions after ischemic preconditioning contributes to tolerance induction after ischemic stroke
Authors
Shin, Jin A.Kim, Yul A.Jeong, Sae ImLee, Kyung-EunKim, Hee-SunPark, Eun-Mi
Ewha Authors
이경은김희선박은미
SCOPUS Author ID
이경은scopus; 김희선scopus; 박은미scopus
Issue Date
2015
Journal Title
BRAIN STRUCTURE & FUNCTION
ISSN
1863-2653JCR Link1863-2661JCR Link
Citation
vol. 220, no. 1, pp. 13 - 26
Keywords
Blood-brain barrierERK1/2Ischemic preconditioningIschemic strokeTight junction proteinsU0126
Publisher
SPRINGER HEIDELBERG
Indexed
SCI; SCIE; SCOPUS WOS
Abstract
Less disruption of the blood-brain barrier (BBB) after severe ischemic stroke is one of the beneficial outcomes of ischemic preconditioning (IP). However, the effect of IP on tight junctions (TJs), which regulate paracellular permeability of the BBB, is not well understood. In the present study, we examined IP-induced changes in TJs before and after middle cerebral artery occlusion (MCAO) in mice, and the association between changes in TJs and tolerance to a subsequent insult. After IP, we found decreased levels of transmembrane TJ proteins occludin and claudin-5, and widened gaps of TJs with perivascular swelling at the ultrastructural level in the brain. An inflammatory response was also observed. These changes were reversed by inhibition of extracellular signal-regulated kinase1/2 (ERK1/2) via the specific ERK1/2 inhibitor U0126. After MCAO, reduced brain edema and inflammatory responses were associated with altered levels of angiogenic factors and cytokines in preconditioned brains. Pretreatment with U0126 reversed the neuroprotective effects of IP against MCAO. These findings suggest that ERK1/2 activation has a pivotal role in IP-induced changes in TJs and inflammatory response, which serve to protect against BBB breakdown and inflammation after ischemic stroke.
DOI
10.1007/s00429-013-0632-5
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE