Angiotensin II does not influence expression of sarcoplasmic reticulum Ca2+ ATPase in atrial myocytes

Cho Kai Wu, Chuen Den Tseng, Yin Tsen Huang, Chia Shan Hsieh, Wei Shan Tsai, Jiunn Lee Lin, Fu Tien Chiang, Chia Ti Tsai

研究成果: 雜誌貢獻文章

1 引文 (Scopus)

摘要

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.
原文英語
頁(從 - 到)121-126
頁數6
期刊JRAAS - Journal of the Renin-Angiotensin-Aldosterone System
10
發行號3
DOIs
出版狀態已發佈 - 九月 10 2009
對外發佈Yes

指紋

Calcium-Transporting ATPases
Sarcoplasmic Reticulum
Angiotensin II
Muscle Cells
Gene Expression
Messenger RNA
Proteins
Gene Expression Regulation
Luciferases
Cardiac Myocytes
Genetic Promoter Regions
Atrial Fibrillation
Genes
Reverse Transcription
Western Blotting
Calcium
Polymerase Chain Reaction

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology

引用此文

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.

於: JRAAS - Journal of the Renin-Angiotensin-Aldosterone System, 卷 10, 編號 3, 10.09.2009, p. 121-126.

研究成果: 雜誌貢獻文章

Wu, Cho Kai ; Tseng, Chuen Den ; Huang, Yin Tsen ; Hsieh, Chia Shan ; Tsai, Wei Shan ; Lin, Jiunn Lee ; Chiang, Fu Tien ; Tsai, Chia Ti. / Angiotensin II does not influence expression of sarcoplasmic reticulum Ca2+ ATPase in atrial myocytes. 於: JRAAS - Journal of the Renin-Angiotensin-Aldosterone System. 2009 ; 卷 10, 編號 3. 頁 121-126.
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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.",
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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

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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.

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