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Acta Physiologica Congress

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Acta Physiologica 2013; Volume 207, Supplement 694
92nd Annual Meeting of the German Physiological Society
3/2/2013-3/5/2013
Heidelberg, Germany


AMP-ACTIVATED PROTEIN KINASE REGULATES HERG POTASSIUM CHANNEL
Abstract number: P098

Almilaji 1   *A. , Munoz 1  C., Elvira 1  B., Pakladok 1  T., Lang 1  F., Föller 1  M.

1 University of Tuebingen, Department of Physiology, Tuebingen, Germany

Background:

AMP-dependent protein kinase (AMPK), a serine-/threonine kinase stimulates energy-generating and inhibits energy-consuming processes thereby helping cardiomyocytes to survive acute energy depletion. The human ether-a-go-go-related gene potassium (hERG) channel contributes to cardiac repolarization and is downregulated in cardiac hypertrophy which predisposes cardiomyocytes to energy depletion. The present study tested whether AMPK regulates hERG channel activity.

Methods:

Wild type AMPK (α1β1γ1), constitutively-active γR70QAMPK (α1β1γ1(R70Q)), or catalytically-inactive aK45RAMPK (α1(K45R)β1γ1) were expressed in Xenopus oocytes with hERG. The voltage-gated current was determined as a measure of hERG channel activity using the two-electrode-voltage clamp. hERG membrane expression was determined by Western Blotting and by chemiluminescence.

Results:

Coexpression of wild type AMPK and of constitutively-active γR70QAMPK significantly down-regulated the voltage-gated current in hERG-expressing Xenopus oocytes. Pharmacological activation of AMPK with AICAR or with phenformin inhibited hERG activity in Xenopus oocytes, an effect abrogated by AMPK inhibitor compound C. Coexpression of constitutively-active γR70QAMPK decreased membrane expression of hERG in Xenopus oocytes.

Conclusions:

AMPK down-regulates hERG-mediated currents. This effect is at least in part due to decreased membrane expression of hERG. AMPK-dependent regulation of hERG may be relevant for downregulation of hERG in cardiac hypertrophy.

To cite this abstract, please use the following information:
Acta Physiologica 2013; Volume 207, Supplement 694 :P098

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