Author + information
- Received August 12, 1994
- Revision received February 28, 1995
- Accepted March 2, 1995
- Published online July 1, 1995.
- Masato Tanaka, MDa,
- Michiaki Hiroe, MDa,*,
- Hiroshi Ito, MDa,
- Toshio Nishikawa, MDa,*,
- Susumu Adachi, MDa,
- Kazutaka Aonuma, MDa and
- Fumiaki Marumo, MDa
- ↵*Address for correspondence: Dr. Michiaki Hiroe, Division of Cardiology, The Second Department of Internal Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113, Japan.
Objectives. This study was designed to determine whether atrial natriuretic peptide and skeletal alpha-actin messenger RNAs (mRNAs) are co-localized in ventricular myocytes of patients with dilated cardiomyopathy.
Background. Atrial natriuretic peptide and skeletal alpha-actin are known as augmented genes with cardiac hypertrophy. However, the expression and localization of both genes in chronic failing heart remain unclear.
Methods. Left ventricular biopsy specimens were obtained from 14 patients with dilated cardiomyopathy. Atrial natriuretic peptide and skeletal alpha-actin mRNAs were detected by in situ hybridization with specific sulfur-35 uridine triphosphate-labeled RNA probes in the serial sections.
Results. Atrial natriuretic peptide mRNA was detected in 10 patients, and intense signals were localized in the myocytes located in the subendocardium and around the interstitial fibrous area. By contrast, skeletal alpha-actin mRNA was homogeneously detected in all myocytes in seven patients. By left ventriculography, patients with skeletal alpha-actin-positive findings had a lower ejection fraction (37.1 ± 6.0%) than those with negative findings (46.3 ± 5.8%, p < 0.05), but atrial natriuretic peptide mRNA expression was not related to left ventricular function.
Conclusions. These results indicate that the expression of atrial natriuretic peptide and skeletal alpha-actin mRNAs are not always co-localized in the left ventricle of patients with dilated cardiomyopathy and suggest that the mechanisms of the regulation of these two genes in the chronic failing heart are different.
This study was supported in part by a Research Grant for Intractable Diseases from the Japanese Ministry of Health and Welfare, by Grants-in-Aid 04670560, 6470522 for General Scientific Research from the Ministry of Education and by an Open Research Grant from The Japan Research Promotion Society for Cardiovascular Disease, Tokyo, Japan.
- Received August 12, 1994.
- Revision received February 28, 1995.
- Accepted March 2, 1995.
- The American College of Cardiology