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.
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Authors | Mayilvahanan Shanmugam, Cristina E Molina, Shumin Gao, Renaud Severac-Bastide, Rodolphe Fischmeister, Gopal J Babu |
Journal | Biochemical and biophysical research communications
(Biochem Biophys Res Commun)
Vol. 410
Issue 1
Pg. 97-101
(Jun 24 2011)
ISSN: 1090-2104 [Electronic] United States |
PMID | 21640081
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2011 Elsevier Inc. All rights reserved. |
Chemical References |
- Muscle Proteins
- Proteolipids
- sarcolipin
- Calcium
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Topics |
- Adult
- Aged
- Aged, 80 and over
- Animals
- Atrial Fibrillation
(metabolism)
- Calcium
(metabolism)
- Disease Models, Animal
- Down-Regulation
- Female
- Heart Atria
(metabolism)
- Humans
- Ion Transport
- Male
- Mice
- Mice, Inbred C57BL
- Middle Aged
- Muscle Proteins
(biosynthesis, genetics)
- Proteolipids
(biosynthesis, genetics)
- Sarcoplasmic Reticulum
(metabolism)
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