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Antiapoptotic and anti-inflammatory mechanisms of heat-shock protein protection

Authors
 MIDORI A. YENARI  ;  JIALING LIU  ;  ZHEN ZHENG  ;  ZINAIDA S. VEXLER  ;  JONG EUN LEE  ;  RONA G. GIFFARD 
Citation
 ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, Vol.1053 : 74-83, 2005 
Journal Title
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
ISSN
 0077-8923 
Issue Date
2005
MeSH
Animals ; Anti-Inflammatory Agents/pharmacology* ; Apoptosis/drug effects* ; HSP70 Heat-Shock Proteins/biosynthesis ; HSP70 Heat-Shock Proteins/pharmacology ; Heat-Shock Proteins/biosynthesis ; Heat-Shock Proteins/pharmacology* ; Heat-Shock Proteins/physiology ; Humans ; Neuroprotective Agents*
Keywords
16179510
Abstract
We and others have previously shown that heat-shock proteins (HSPs) are involved in protecting the brain from a variety of insults including stroke, epilepsy, and other related insults. While the mechanism of this protection has largely been thought to be due to their chaperone functions (i.e., preventing abnormal protein folding or aggregation), recent work has shown that HSPs may also directly interfere with other cell death pathways such as apoptosis and inflammation. Using models of cerebral ischemic and ischemia-like injury, we overexpressed the 70-kDa heat-shock protein (HSP70) using gene transfer or by studying a transgenic mouse model. HSP70 protected neurons and astrocytes from experimental stroke and stroke-like insults. HSP70 transgenic mice also had better neurological scores following experimental stroke compared to their wild-type littermates. Overexpressing HSP70 was associated with less apoptotic cell death and increased expression of the antiapoptotic protein, Bcl-2. Furthermore, HSP70 suppressed microglial/monocyte activation following experimental stroke. HSP70 overexpression also led to the reduction of matrix metalloproteinases. We suggest that HSPs are capable of protecting brain cells from lethal insults through a variety of mechanisms and should be explored as a potential therapy against stroke and other neurodegenerative diseases.
Full Text
http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.2005.tb00012.x/abstract
DOI
10.1196/annals.1344.007
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Anatomy (해부학교실) > 1. Journal Papers
Yonsei Authors
Lee, Jong Eun(이종은) ORCID logo https://orcid.org/0000-0001-6203-7413
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/151167
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