Document Detail


Bilirubin oxidation end products directly alter K+ channels important in the regulation of vascular tone.
MedLine Citation:
PMID:  20424637     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The exact etiology of delayed cerebral vasospasm following cerebral hemorrhage is not clear, but a family of compounds termed 'bilirubin oxidation end products (BOXes)' derived from heme has been implicated. As proper regulation of vascular smooth muscle tone involves large-conductance Ca(2+)- and voltage-dependent Slo1 K(+) (BK, maxiK, K(Ca)1.1) channels, we examined whether BOXes altered functional properties of the channel. Electrophysiological measurements of Slo1 channels heterologously expressed in a human cell line and of native mouse BK channels in isolated cerebral myocytes showed that BOXes markedly diminished open probability. Biophysically, BOXes specifically stabilized the conformations of the channel with its ion conduction gate closed. The results of chemical amino-acid modifications and molecular mutagenesis together suggest that two specific lysine residues in the structural element linking the transmembrane ion-permeation domain to the carboxyl cytosolic domain of the Slo1 channel are critical in determining the sensitivity of the channel to BOXes. Inhibition of Slo1 BK channels by BOXes may contribute to the development of delayed cerebral vasospasm following brain hemorrhage.
Authors:
Shangwei Hou; Rong Xu; Joseph F Clark; William L Wurster; Stefan H Heinemann; Toshinori Hoshi
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-04-28
Journal Detail:
Title:  Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism     Volume:  31     ISSN:  1559-7016     ISO Abbreviation:  J. Cereb. Blood Flow Metab.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-04     Completed Date:  2011-02-03     Revised Date:  2012-01-04    
Medline Journal Info:
Nlm Unique ID:  8112566     Medline TA:  J Cereb Blood Flow Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  102-12     Citation Subset:  IM    
Affiliation:
Department of Physiology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
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MeSH Terms
Descriptor/Qualifier:
Algorithms
Amino Acid Sequence
Animals
Basilar Artery / drug effects,  metabolism
Bilirubin / cerebrospinal fluid,  metabolism,  physiology*
Cerebrovascular Circulation / physiology*
Electrophysiological Phenomena
Humans
Kinetics
Large-Conductance Calcium-Activated Potassium Channel alpha Subunits / drug effects,  metabolism,  physiology*
Mice
Mice, Inbred C57BL
Molecular Sequence Data
Muscle Tonus / physiology
Muscle, Smooth, Vascular / physiology*
Oxidation-Reduction
Patch-Clamp Techniques
Potassium Channel Blockers / pharmacology
Vasospasm, Intracranial / physiopathology
Grant Support
ID/Acronym/Agency:
GM057654/GM/NIGMS NIH HHS; NS050569/NS/NINDS NIH HHS; R01 GM057654-13/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/KCNMA1 protein, human; 0/Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; 0/Potassium Channel Blockers; 635-65-4/Bilirubin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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