Slow Cardiac Myosin Regulatory Light Chain 2 (MYL2) was Down-Expressed in Chronic Heart Failure Patients
Article first published online: 10 DEC 2010
Copyright © 2010 Wiley Periodicals, Inc.
Volume 34, Issue 1, pages 30–34, January 2011
How to Cite
Li, Y., Wu, G., Tang, Q., Huang, C., Jiang, H., Shi, L., Tu, X., Huang, J., Zhu, X. and Wang, H. (2011), Slow Cardiac Myosin Regulatory Light Chain 2 (MYL2) was Down-Expressed in Chronic Heart Failure Patients. Clin Cardiol, 34: 30–34. doi: 10.1002/clc.20832
- Issue published online: 21 JAN 2011
- Article first published online: 10 DEC 2010
Genetic studies have shown that many slow cardiac myosin regulatory light chain 2 (MYL2) gene mutations can cause hypertrophic cardiomyopathy, which is one of the most common causes of heart failure (HF). But until now there has been no pathological or histological evidence that MYL2 may be associated with HF development. Recent microarray studies indicated that myosin heavy chain expression changed in the pathological process of HF. Because MYL2 is a regulatory component of myosin heavy polypeptide, the role of MYL2 protein in HF needs to be studied.
The level of expression of MYL2 may change in the heart tissue of patients with chronic HF.
We collected 28 human right auricle samples, 16 from chronic HF patients and 12 from healthy control subjects. Immunohistochemistry was carried out to observe the tissue-expression pattern of the MYL2 protein and Western blot methods were performed to quantify the relative MYL2 expression level.
In chronic HF patients, the MYL2 protein level decreased significantly compared with normal controls (t test P < 0.05). Among the 16 HF patients, MYL2 expression in the severe HF group (New York Heart Association [NYHA] class III or IV) was even lower than that of the moderate HF group (NYHA class II) (t test P < 0.05).
MYL2 was down-expressed in HF tissues, and our findings suggested that MYL2 may play a role in the development and progression of chronic HF. Copyright © 2008 Wiley Periodicals, Inc.
The first two authors contributed equally to this work. This study was supported by the National Natural Science Foundation of China (30800457, 30900803) and the Natural Science Program of Hubei Province (2009CDZ013). This study has no relationship with any kind of industry. The authors have no other funding, financial relationships, or conflicts of interest to disclose.