| Home  | About ScienceAsia  | Publication charge  | Advertise with us  | Subscription for printed version  | Contact us  
Editorial Board
Journal Policy
Instructions for Authors
Online submission
Author Login
Reviewer Login
Volume 50 Number 1
Volume 49 Number 6
Volume 49 Number 5
Volume 49S Number 1
Volume 49 Number 4
Volume 49 Number 3
Earlier issues
Back

Research Articles

ScienceAsia 33 (2007): 265-271 |doi: 10.2306/scienceasia1513-1874.2007.33.265

ATF3 Transgenic Mice: Structural Analysis of Cardiac Myocytes


Wuthichai Klomkleawa*, Prasarn Tangkawattanab, Tsonwin Haic, Yoshichika Okamotoc, Makoto Mutod and Mamoru Yamaguchie

 
ABSTRACT:     Over-expression of the activating transcription factor 3 (ATF3) in transgenic (TG) mice induces atrial enlargement. This manuscript reports anatomical and structural alterations in TG mice hearts. A statistical analysis showed that hearts of the TG mice (0.61±0.2 grams) are significantly heavier than those of non-transgenic (nTG) mice (0.16±0.03 grams) (P<0.05). The average myocyte cross-sectional area of the TG mice (172.51±72.72 μm2) was significantly larger than that of nTG mice (74.4±16.46 μm2) (P<0.05). The alterations varied greatly among individual atria, with and without visible calcification. Approximately 56% of TG mice produced recognizable calcification in the right atrium. Moreover, very few apoptotic cells were observed. Ultrastructural studies of the enlarged atria showed 1) degeneration and degradation of cytoplasmic components and mineralization of mitochondria leading to total destruction and death of myocytes, 2) hyperchromatic-hypertrophic nuclei with various nuclear inclusions, 3) fibrosis and mineralization of the myocardial layer, and 4) thrombus, cartilage and bone formation. It is possible that cellular injury would cause energy metabolism impairment and/or sarcolemmal malformation leading to Ca++ accumulation and subsequent ultrastructural changes. Although pathogenesis of this alteration remains unclear, ATF3 could be involved in these abnormalities.

Download PDF


a Department of Veterinary Anatomy, Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand.
b Department of Veterinary Anatomy, Faculty of Veterinary Medicine, Khon Kaen University, Khon Kaen, Thailand.
c Department of Molecular and Cellular Biochemistry and Center for Molecular Neurobiology, The Ohio State University, Columbus, Ohio, USA.
d Department of Veterinary Surgery, School of Veterinary Medicine, Azabu University, Kanagawa, Japan.
e Department of Veterinary Biosciences, College of Veterinary Medicine, The Ohio State University, Columbus, Ohio, USA.

* Corresponding author, E-mail: Wuthichai.K@Chula.ac.th

Received 15 Feb 2006, Accepted 9 Jan 2007