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

Department of Internal Medicine, National Taiwan University College of Medicine and Hospital Yun-Lin Branch, Yun-Lin, Taiwan

Chuen-Den Tseng

Division of Cardiology, Department of Internal Medicine, National Taiwan University College of Medicine and Hospital, Taipei, Taiwan, cdtseng{at}ntu.edu.tw

Yin-Tsen Huang

Department of Family Medicine, Mackay Memorial Hospital, Taipei, Taiwan, fang31{at}ms39.hinet.net

Chia-Shan Hsieh

Division of Cardiology, Department of Internal Medicine, National Taiwan University College of Medicine and Hospital, Taipei, Taiwan

Wei-Shan Tsai

Department of Internal Medicine, National Taiwan University College of Medicine and Hospital Yun-Lin Branch, Yun-Lin, Taiwan

Jiunn-Lee Lin

Division of Cardiology, Department of Internal Medicine, National Taiwan University College of Medicine and Hospital, Taipei, Taiwan

Fu-Tien Chiang

Division of Cardiology, Department of Internal Medicine, National Taiwan University College of Medicine and Hospital, Taipei, Taiwan, Department of Laboratory Medicine, National Taiwan University Hospital, Taipei, Taiwan

Chia-Ti Tsai

Division of Cardiology, Department of Internal Medicine, National Taiwan University College of Medicine and Hospital, Taipei, Taiwan

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.

Key Words: angiotensin II • HL-1 cardiomyocytes • promoter • sarcoplasmic reticulum Ca2+ ATPase • transcriptional regulation

This version was published on September 1, 2009

Journal of Renin-Angiotensin-Aldosterone System, Vol. 10, No. 3, 121-126 (2009)
DOI: 10.1177/1470320309342732


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