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Angiotensin II does not influence expression of sarcoplasmic reticulum Ca2 + ATPase in atrial myocytes
Author(s) -
Cho Kai Wu,
Chuen Den Tseng,
Yin Tsen Huang,
Chia Shan Hsieh,
Wei-Shan Tsai,
Jiunn Lee Lin,
Fu-Tien Chiang,
Chien-Hung Tsai
Publication year - 2009
Publication title -
jraas. journal of the renin-angiotensin-aldosterone system/journal of the renin-angiotensin-aldosterone system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.457
H-Index - 46
eISSN - 1752-8976
pISSN - 1470-3203
DOI - 10.1177/1470320309342732
Subject(s) - serca , myocyte , medicine , endoplasmic reticulum , angiotensin ii , chemistry , gene expression , endocrinology , atrial myocytes , atrial fibrillation , western blot , biology , gene , atpase , receptor , enzyme , biochemistry
. The sarcoplasmic reticulum Ca 2+ ATPase (SERCA) is essential for the regulation of the intracellular calcium level in cardiomyocytes. Previous studies have found that angiotensin II (Ang II) decreased SERCA2 gene expression in ventricular myocytes. Alteration of SERCA activity is important in the mechanism of atrial fibrillation. The present study was undertaken to examine Ang II effects on atrial myocytes. Materials and methods. An ~1.75-kb promoter region of SERCA2 gene was cloned with the pGL3 luciferase vector. The direct effects of Ang II on SERCA2 gene expression in HL-1 atrial myocytes were examined by promoter activity assay, followed by Western blot analysis for protein levels and quantitative real-time reverse transcription polymerase chain reaction for mRNA amounts. Results. Ang II did not increase the promoter activity of the 1,754-bp promoter-receptor construct of the SERCA2 gene. The levels of SERCA2 protein and mRNA were also unchanged at different time points after Ang II treatment. Conclusions. Although Ang II had prominent effects on SERCA2 in ventricular myocytes, it did not alter SERCA2 gene expression and protein levels in atrial myocytes. We provide a model for further investigation of the regulation of SERCA2 gene expression in atrial myocytes.

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