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J. Biol. Chem., Vol. 278, Issue 11, 9570-9575, March 14, 2003
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From the Intracellular Ca2+ regulation
is critical in the normal cardiac function and development of
pathologic hearts. Phospholamban, an endogenous inhibitor of
sarcoplasmic reticulum Ca2+ ATPase in the sarcoplasmic
reticulum, plays an important role in Ca2+ cycling in
heart. Recently, sarcolipin has been identified as having a similar
function as phospholamban in skeletal muscle. Because phospholamban is
differentially expressed in atrial and ventricular myocardia and its
expression is often altered in diseased hearts, we investigated the
cardiac chamber specificity of sarcolipin expression and its regulation
during development and hypertrophic remodeling. Northern blot analysis
revealed that the expression of mouse sarcolipin mRNA was most
abundant in the atria and was undetectable in the ventricles,
indicating an atrial chamber-specific expression pattern. Atrial
chamber-specific expression of sarcolipin mRNA was increased during
development. These findings were confirmed by in situ
hybridization studies. In addition, sarcolipin expression was
down-regulated in the atria of hypertrophic heart when induced by
ventricular specific overexpression of the activated
H-ras gene. In humans, sarcolipin mRNA was
also expressed in the atria but not detected in the ventricles,
although sarcolipin expression was most abundant in skeletal muscle.
Taken together, sarcolipin is likely to be an atrial chamber-specific
regulator of Ca2+ cycling in heart.
Atrial Chamber-specific Expression of
Sarcolipin Is Regulated during Development and Hypertrophic
Remodeling*
§¶,
,,¶§§
Department of Pediatric Cardiology and the
§§ Division of Genomic Medicine, Institute of Advanced
Biomedical Engineering and Science, Graduate School of Medicine, Tokyo
Women's Medical University, Tokyo 162-8666, Japan, the
§ Department of Physiology, Yokohama City University School
of Medicine, Yokohama, 236-0004 Japan, the Department of
Physiology, University of Maryland School of Medicine, Baltimore,
Maryland 21201, the ** Institute of Molecular Medicine,
University of California at San Diego, La Jolla, California 92093, and the Department of Cell Biology and Molecular
Medicine, New Jersey Medical School, Newark, New Jersey 07103
*
This work was supported in part by an open research grant
from the Japan Research Promotion Society for Cardiovascular Diseases (2001).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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