Atrial natriuretic peptide inhibits cardiomyocyte hypertrophy through mitogen-activated protein kinase phosphatase-1
| Autor: | Yasushi Imai, Ryozo Nagai, Yunzeng Zou, Yoshio Yazaki, Masaki Shimoyama, Koichiro Harada, Koshiro Monzen, Doubun Hayashi, Issei Komuro, Ichiro Shiojima, Sumiyo Kudoh, Tsutomu Yamazaki |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
MAPK/ERK pathway
medicine.medical_specialty medicine.medical_treatment Biophysics Cardiomegaly Cell Cycle Proteins Biology Biochemistry Immediate-Early Proteins Atrial natriuretic peptide Protein Phosphatase 1 Internal medicine Phosphoprotein Phosphatases medicine Animals Myocyte Myocytes Cardiac Rats Wistar Protein kinase A Molecular Biology Cells Cultured Dose-Response Relationship Drug Growth factor Dual Specificity Phosphatase 1 Protein phosphatase 1 Cell Biology Endothelin 1 Angiotensin II Rats Endocrinology Animals Newborn cardiovascular system Mitogen-Activated Protein Kinases Protein Tyrosine Phosphatases Atrial Natriuretic Factor hormones hormone substitutes and hormone antagonists Signal Transduction circulatory and respiratory physiology |
| Zdroj: | Biochemical and Biophysical Research Communications. 322:310-319 |
| ISSN: | 0006-291X |
| DOI: | 10.1016/j.bbrc.2004.07.119 |
| Popis: | Cardiac hypertrophy is formed in response to hemodynamic overload. Although a variety of factors such as catecholamines, angiotensin II (AngII), and endothelin-1 (ET-1) have been reported to induce cardiac hypertrophy, little is known regarding the factors that inhibit the development of cardiac hypertrophy. Production of atrial natriuretic peptide (ANP) is increased in the hypertrophied heart and ANP has recently been reported to inhibit the growth of various cell types. We therefore examined whether ANP inhibits the development of cardiac hypertrophy. Pretreatment of cultured cardiomyocytes with ANP inhibited the AngII- or ET-1-induced increase in the cell size and the protein synthesis. ANP also inhibited the AngII- or ET-1-induced hypertrophic responses such as activation of mitogen-activated protein kinase (MAPK) and induction of immediate early response genes and fetal type genes. To determine how ANP inhibits cardiomyocyte hypertrophy, we examined the mechanism of ANP-induced suppression of the MAPK activation. ANP strongly induced expression of MAPK phosphatase-1 (MKP-1) and overexpression of MKP-1 inhibited AngII- or ET-1-induced hypertrophic responses. These growth-inhibitory actions of ANP were mimicked by a cyclic GMP analog 8-bromo-cyclic GMP. Taken together, ANP directly inhibits the growth factor-induced cardiomyocyte hypertrophy at least partly via induction of MKP-1. Our present study suggests that the formation of cardiac hypertrophy is regulated not only by positive but by negative factors in response to hemodynamic load. |
| Databáze: | OpenAIRE |
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