Suppression of deltaPKC activation after focal cerebral ischemia contributes to the protective effect of hypothermia.

Suppression of deltaPKC activation after focal cerebral ischemia contributes to the protective effect of hypothermia. Research Abstract Details 

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Suppression of deltaPKC activation after focal cerebral ischemia contributes to the protective effect of hypothermia. Abstract Text:

Takayoshi Shimohata,Heng Zhao,Jae Hoon Sung,Guohua Sun,Daria Mochly-Rosen,Gary K Steinberg,

Mild hypothermia is a robust neuroprotective treatment for stroke. Understanding the mechanisms underlying hypothermia's benefits will lead to more effective treatments to prevent stroke damage. Delta protein kinase C (deltaPKC) is a kinase that has been strongly implicated in executing ischemic damage. We investigated the effects of hypothermia on deltaPKC activation, as determined by its subcellular translocation, proteolytic cleavage, and phosphorylation in a focal cerebral ischemia model. The amount of constitutively activated C-terminal catalytic fragment of deltaPKC (CF-deltaPKC) increased after stroke. Both hypothermia (30 degrees C) and the caspase-3-specific inhibitor, Z-DQMD-FMK, blocked the accumulation of activated deltaPKC in the penumbra. Other hallmarks of deltaPKC activation, its translocation to the mitochondria, and nucleus were observed in the penumbra as early as 10 mins after reperfusion. These events were blocked by hypothermia. Hypothermia also blocked CF-deltaPKC increases in the mitochondria and nuclei. Conversely, a specific deltaPKC activator, psideltaRACK, decreased the neuroprotective effect of hypothermia. Finally, deltaPKC activity may lead to mitochondrial injury and cytochrome c release, as the timing of cytochrome c release corresponded to the time course of deltaPKC translocation. Both cytochrome c release and deltaPKC translocation were blocked by hypothermia. In conclusion, hypothermia protects against ischemic damage in part by suppressing deltaPKC activation after stroke.

Suppression of deltaPKC activation after focal cerebral ischemia contributes to the protective effect of hypothermia. Publishing Authors By Initials

T Shimohata,H Zhao,JH Sung,G Sun,D Mochly-Rosen,GK Steinberg,

For similar proteins: membrane proteins: receptors, cell surface research abstracts see: proteins: membrane proteins: receptors, cell surface research

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Suppression of deltaPKC activation after focal cerebral ischemia contributes to the protective effect of hypothermia. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of cerebral blood flow and metabolism : of

VOLUME: 27

Page Numbers: 1463-75

Journal Abbreviation: J. Cereb. Blood Flow Metab.

ISSN: 0271-678X

DAY: 7

MONTH: 02

YEAR: 2007

Suppression of deltaPKC activation after focal cerebral ischemia contributes to the protective effect of hypothermia. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8112566

Suppression of deltaPKC activation after focal cerebral ischemia contributes to the protective effect of hypothermia. Keywords Mesh Terms:

KEYWORDS: Receptors, Cell Surface

MESH TERMS: metabolism

Chemical & Substance for Abstract: Suppression of deltaPKC activation after focal cerebral ischemia contributes to the protective effect of hypothermia. Information

Substance Name: Caspase 3

Registry Number: EC 3.4.22.-

Grant and Affiliation Information for Suppression of deltaPKC activation after focal cerebral ischemia contributes to the protective effect of hypothermia.

AFFILIATION: Department of Neurosurgery, Stanford University, Stanford, California 94305-5327, USA.

Country: United States

AGENCY: United States NINDS

GRANT: R01 NS27292

ACRONYM: NS

MEDLINETA: J Cereb Blood Flow Metab

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