Overexpression of SUR2A generates a cardiac phenotype resistant to ischemia.

Overexpression of SUR2A generates a cardiac phenotype resistant to ischemia. Research Abstract Details 

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Overexpression of SUR2A generates a cardiac phenotype resistant to ischemia. Abstract Text:

Qingyou Du,Sofija Jovanovi?,Allyson Clelland,Andrey Sukhodub,Grant Budas,Karen Phelan,Victoria Murray-Tait,Lorraine Malone,Aleksandar Jovanovi?,

ATP-sensitive K+ (K(ATP)) channels are present in the sarcolemma of cardiac myocytes where they link membrane excitability with the cellular bioenergetic state. These channels are in vivo composed of Kir6.2, a pore-forming subunit, SUR2A, a regulatory subunit, and at least four accessory proteins. In the present study, real-time RT-PCR has demonstrated that of all six sarcolemmal K(ATP) channel-forming proteins, SUR2A was probably the least expressed protein. We have generated mice where the SUR2A was under the control of a cytomegalovirus promoter, a promoter that is more efficient than the native promoter. These mice had an increase in SUR2A mRNA/protein levels in the heart whereas levels of mRNAs of other channel-forming proteins were not affected at all. Imunoprecipitation/Western blot and patch clamp electrophysiology has shown an increase in K(ATP) channel numbers in the sarcolemma of transgenic mice. Cardiomyocytes from transgenic mice responded to hypoxia with shortening of action membrane potential and were significantly more resistant to this insult than cardiomyocytes from the wild-type. The size of myocardial infarction in response to ischemia-reperfusion was much smaller in hearts from transgenic mice compared to those in wild-type. We conclude that overexpression of SUR2A generates cardiac phenotype resistant to hypoxia/ischemia/reperfusion injury due at least in part to increase in levels of sarcolemmal K(ATP) channels.

Overexpression of SUR2A generates a cardiac phenotype resistant to ischemia. Publishing Authors By Initials

Q Du,S Jovanovi?,A Clelland,A Sukhodub,G Budas,K Phelan,V Murray-Tait,L Malone,A Jovanovi?,

For similar cells: cellular structures: cell membrane: sarcolemma research abstracts see: cells: cellular structures: cell membrane: sarcolemma research

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Overexpression of SUR2A generates a cardiac phenotype resistant to ischemia. Journal Published:

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

Journal: The FASEB journal : official publication of the Fe

VOLUME: 20

Page Numbers: 1131-41

Journal Abbreviation: FASEB J.

ISSN: 1530-6860

DAY: 11

MONTH: Jun

YEAR: 2006

Overexpression of SUR2A generates a cardiac phenotype resistant to ischemia. Information

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LANGUAGE: eng

NlmUniqueID: 8804484

Overexpression of SUR2A generates a cardiac phenotype resistant to ischemia. Keywords Mesh Terms:

KEYWORDS: Sarcolemma

MESH TERMS: metabolism

Chemical & Substance for Abstract: Overexpression of SUR2A generates a cardiac phenotype resistant to ischemia. Information

Substance Name: sulfonylurea receptor

Registry Number: 0

Grant and Affiliation Information for Overexpression of SUR2A generates a cardiac phenotype resistant to ischemia.

AFFILIATION: Maternal and Child Health Sciences, Ninewells Hospital & Medical School, University of Dundee, Dundee, DD1 9SY Scotland, UK.

Country: United States

AGENCY: United Kingdom Wellcome T

GRANT: S18744

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MEDLINETA: FASEB J

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