Decreased sarcolipin protein expression and enhanced sarco(endo)plasmic reticulum Ca2+ uptake in human atrial fibrillation

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Decreased sarcolipin protein expression and enhanced sarco(endo)plasmic reticulum Ca2+ uptake in human atrial fibrillation. / Shanmugam, Mayilvahanan; Molina, Cristina E; Gao, Shumin; Severac-Bastide, Renaud; Fischmeister, Rodolphe; Babu, Gopal J.

in: BIOCHEM BIOPH RES CO, Jahrgang 410, Nr. 1, 24.06.2011, S. 97-101.

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@article{e4af1badba9a4bafb92846f8c0f04e35,
title = "Decreased sarcolipin protein expression and enhanced sarco(endo)plasmic reticulum Ca2+ uptake in human atrial fibrillation",
abstract = "Sarcolipin (SLN), a key regulator of cardiac sarco(endo)plasmic reticulum (SR) Ca(2+) ATPase, is predominantly expressed in atria and mediates β-adrenergic responses. Studies have shown that SLN mRNA expression is decreased in human chronic atrial fibrillation (AF) and in aortic banded mouse atria; however, SLN protein expression in human atrial pathology and its role in atrial SR Ca(2+) uptake are not yet elucidated. In the present study, we determined the expression of major SR Ca(2+) handling proteins in atria of human AF patients and in human and in a mouse model of heart failure (HF). We found that the expression of SR Ca(2+) uptake and Ca(2+) release channel proteins are significantly decreased in atria but not in the ventricles of pressure-overload induced HF in mice. In human AF and HF, the expression of SLN protein was significantly decreased; whereas the expressions of other major SR Ca(2+) handling proteins were not altered. Further, we found that the SR Ca(2+) uptake was significantly increased in human AF. The selective downregulation of SLN and enhanced SR Ca(2+) uptake in human AF suggest that SLN downregulation could play an important role in abnormal intracellular Ca(2+) cycling in atrial pathology.",
keywords = "Adult, Aged, Aged, 80 and over, Animals, Atrial Fibrillation, Calcium, Disease Models, Animal, Down-Regulation, Female, Heart Atria, Humans, Ion Transport, Male, Mice, Mice, Inbred C57BL, Middle Aged, Muscle Proteins, Proteolipids, Sarcoplasmic Reticulum, Journal Article, Research Support, Non-U.S. Gov't",
author = "Mayilvahanan Shanmugam and Molina, {Cristina E} and Shumin Gao and Renaud Severac-Bastide and Rodolphe Fischmeister and Babu, {Gopal J}",
note = "Copyright {\textcopyright} 2011 Elsevier Inc. All rights reserved.",
year = "2011",
month = jun,
day = "24",
doi = "10.1016/j.bbrc.2011.05.113",
language = "English",
volume = "410",
pages = "97--101",
journal = "BIOCHEM BIOPH RES CO",
issn = "0006-291X",
publisher = "Academic Press Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - Decreased sarcolipin protein expression and enhanced sarco(endo)plasmic reticulum Ca2+ uptake in human atrial fibrillation

AU - Shanmugam, Mayilvahanan

AU - Molina, Cristina E

AU - Gao, Shumin

AU - Severac-Bastide, Renaud

AU - Fischmeister, Rodolphe

AU - Babu, Gopal J

N1 - Copyright © 2011 Elsevier Inc. All rights reserved.

PY - 2011/6/24

Y1 - 2011/6/24

N2 - Sarcolipin (SLN), a key regulator of cardiac sarco(endo)plasmic reticulum (SR) Ca(2+) ATPase, is predominantly expressed in atria and mediates β-adrenergic responses. Studies have shown that SLN mRNA expression is decreased in human chronic atrial fibrillation (AF) and in aortic banded mouse atria; however, SLN protein expression in human atrial pathology and its role in atrial SR Ca(2+) uptake are not yet elucidated. In the present study, we determined the expression of major SR Ca(2+) handling proteins in atria of human AF patients and in human and in a mouse model of heart failure (HF). We found that the expression of SR Ca(2+) uptake and Ca(2+) release channel proteins are significantly decreased in atria but not in the ventricles of pressure-overload induced HF in mice. In human AF and HF, the expression of SLN protein was significantly decreased; whereas the expressions of other major SR Ca(2+) handling proteins were not altered. Further, we found that the SR Ca(2+) uptake was significantly increased in human AF. The selective downregulation of SLN and enhanced SR Ca(2+) uptake in human AF suggest that SLN downregulation could play an important role in abnormal intracellular Ca(2+) cycling in atrial pathology.

AB - Sarcolipin (SLN), a key regulator of cardiac sarco(endo)plasmic reticulum (SR) Ca(2+) ATPase, is predominantly expressed in atria and mediates β-adrenergic responses. Studies have shown that SLN mRNA expression is decreased in human chronic atrial fibrillation (AF) and in aortic banded mouse atria; however, SLN protein expression in human atrial pathology and its role in atrial SR Ca(2+) uptake are not yet elucidated. In the present study, we determined the expression of major SR Ca(2+) handling proteins in atria of human AF patients and in human and in a mouse model of heart failure (HF). We found that the expression of SR Ca(2+) uptake and Ca(2+) release channel proteins are significantly decreased in atria but not in the ventricles of pressure-overload induced HF in mice. In human AF and HF, the expression of SLN protein was significantly decreased; whereas the expressions of other major SR Ca(2+) handling proteins were not altered. Further, we found that the SR Ca(2+) uptake was significantly increased in human AF. The selective downregulation of SLN and enhanced SR Ca(2+) uptake in human AF suggest that SLN downregulation could play an important role in abnormal intracellular Ca(2+) cycling in atrial pathology.

KW - Adult

KW - Aged

KW - Aged, 80 and over

KW - Animals

KW - Atrial Fibrillation

KW - Calcium

KW - Disease Models, Animal

KW - Down-Regulation

KW - Female

KW - Heart Atria

KW - Humans

KW - Ion Transport

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Middle Aged

KW - Muscle Proteins

KW - Proteolipids

KW - Sarcoplasmic Reticulum

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1016/j.bbrc.2011.05.113

DO - 10.1016/j.bbrc.2011.05.113

M3 - SCORING: Journal article

C2 - 21640081

VL - 410

SP - 97

EP - 101

JO - BIOCHEM BIOPH RES CO

JF - BIOCHEM BIOPH RES CO

SN - 0006-291X

IS - 1

ER -