Abstract
Introduction. The sarcoplasmic reticulum Ca2+ 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.
Original language | English |
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Pages (from-to) | 121-126 |
Number of pages | 6 |
Journal | JRAAS - Journal of the Renin-Angiotensin-Aldosterone System |
Volume | 10 |
Issue number | 3 |
DOIs | |
Publication status | Published - Sep 10 2009 |
Externally published | Yes |
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Keywords
- Angiotensin II
- HL-1 cardiomyocytes
- Promoter
- Sarcoplasmic reticulum Ca ATPase
- Transcriptional regulation
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology
Cite this
Angiotensin II does not influence expression of sarcoplasmic reticulum Ca2+ ATPase in atrial myocytes. / Wu, Cho Kai; Tseng, Chuen Den; Huang, Yin Tsen; Hsieh, Chia Shan; Tsai, Wei Shan; Lin, Jiunn Lee; Chiang, Fu Tien; Tsai, Chia Ti.
In: JRAAS - Journal of the Renin-Angiotensin-Aldosterone System, Vol. 10, No. 3, 10.09.2009, p. 121-126.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Angiotensin II does not influence expression of sarcoplasmic reticulum Ca2+ ATPase in atrial myocytes
AU - Wu, Cho Kai
AU - Tseng, Chuen Den
AU - Huang, Yin Tsen
AU - Hsieh, Chia Shan
AU - Tsai, Wei Shan
AU - Lin, Jiunn Lee
AU - Chiang, Fu Tien
AU - Tsai, Chia Ti
PY - 2009/9/10
Y1 - 2009/9/10
N2 - Introduction. The sarcoplasmic reticulum Ca2+ 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.
AB - Introduction. The sarcoplasmic reticulum Ca2+ 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.
KW - Angiotensin II
KW - HL-1 cardiomyocytes
KW - Promoter
KW - Sarcoplasmic reticulum Ca ATPase
KW - Transcriptional regulation
UR - http://www.scopus.com/inward/record.url?scp=69849098027&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=69849098027&partnerID=8YFLogxK
U2 - 10.1177/1470320309342732
DO - 10.1177/1470320309342732
M3 - Article
C2 - 19617272
AN - SCOPUS:69849098027
VL - 10
SP - 121
EP - 126
JO - JRAAS - Journal of the Renin-Angiotensin-Aldosterone System
JF - JRAAS - Journal of the Renin-Angiotensin-Aldosterone System
SN - 1470-3203
IS - 3
ER -