Detailed Information

Cited 67 time in webofscience Cited 71 time in scopus
Metadata Downloads

Immune following suppression mesenchymal stem cell transplantation in the ischemic brain is mediated by TGF-beta

Authors
Yoo, Seung-WanChang, Da-YoungLee, Hye-SunKim, Gyu-HeePark, Jin-SungRyu, Buom-YongJoe, Eun-HyeLee, Young-DonKim, Sung-SooSuh-Kim, Haeyoung
Issue Date
Oct-2013
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
Stroke; Inflammation; Microglia; Cell death; Mesenchymal stem cell; TGF-beta
Citation
NEUROBIOLOGY OF DISEASE, v.58, pp 249 - 257
Pages
9
Journal Title
NEUROBIOLOGY OF DISEASE
Volume
58
Start Page
249
End Page
257
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/14237
DOI
10.1016/j.nbd.2013.06.001
ISSN
0969-9961
1095-953X
Abstract
Transplantation of mesenchymal stem cells (MSCs) has been shown to enhance the recovery of brain functions following ischemic injury. Although immune modulation has been suggested to be one of the mechanisms, the molecular mechanisms underlying improved recovery has not been clearly identified. Here, we report that MSCs secrete transforming growth factor-beta (TGF-beta) to suppress immune propagation in the ischemic rat brain. Ischemic stroke caused global death of resident cells in the infarcted area, elevated the monocyte chemoattractant protein-1 (MCP-1) level, and evoked massive infiltration of circulating CD68+ immune cells through the impaired blood brain barrier. Transplantation of MSCs at day 3 post-ischemia blocked the subsequent upregulation of MCP-1 in the ischemic area and the infiltration of additional CD68+ immune cells. MSC-conditioned media decreased the migration and MCP-1 production of freshly isolated immune cells in vitro, and this effect was blocked by an inhibitor of TGF-beta signaling or an anti-TGF-beta neutralizing antibody. Finally, transplantation of TGF-beta 1-silenced MSCs failed to attenuate the infiltration of CD68+ cells into the ischemic brain, and was associated with only minor improvements in motor function. These results indicate that TGF-beta is key to the ability of MSCs to beneficially attenuate immune reactions in the ischemic brain. Our findings offer insight into the interactions between allogeneic MSCs and the host immune system, reinforcing the prospective clinical value of using MSCs in the treatment of neurological disorders involving inflammation-mediated secondary damage. (C) 2013 The Authors. Published by Elsevier Inc. All rights reserved.
Files in This Item
There are no files associated with this item.
Appears in
Collections
ETC > 1. Journal Articles

qrcode

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

Related Researcher

Researcher Ryu, Buom-Yong photo

Ryu, Buom-Yong
대학원 (동물생명공학과.)
Read more

Altmetrics

Total Views & Downloads

BROWSE