Molecular mechanism of cardiac cellular hypertrophy by mechanical stress.
Mechanical stress is a major cause of cardiac hypertrophy. Although the mechanisms by which mechanical load induces cardiac cellular hypertrophy have long been a subject of great interest for cardiologists, the lack of a good in vitro system has hampered the understanding of the biochemical mechanisms. For these past several years, however, an in vitro cardiocyte culture system has made it possible to examine the biochemical basis for the signal transduction of mechanical stress. Passive stretch of cardiomyocytes cultured on silicone membranes activates protein kinase cascades of phosphorylation and induces an increase in protein synthesis and the expression of both immediate early genes such as c-fos, c-myc, c-jun, Egr-1, and late response genes such as beta-myosin heavy chain and skeletal alpha-actin. Although an important question regarding how mechanical stimulus is converted into biochemical signals remains unknown, the cultured cardiomyocyte is a good model to examine the signal transduction pathways of mechanical stress.
Yamazaki
T
T
Department of Medicine III, University of Tokyo School of Medicine, Japan.
Komuro
I
I
Yazaki
Y
Y
D000199:Actins / Q000096:biosynthesis; D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism* / Q000503:physiopathology; D002478:Cells, Cultured; D003599:Cytoskeleton / Q000502:physiology / Q000648:ultrastructure; D005109:Extracellular Matrix / Q000502:physiology / Q000648:ultrastructure; D005786:Gene Expression Regulation; D017781:Genes, Immediate-Early; D006801:Humans; D009206:Myocardium / Q000378:metabolism*; D009218:Myosins / Q000096:biosynthesis; D015290:Second Messenger Systems; D015398:Signal Transduction; D013314:Stress, Mechanical
D000199:Actins; D009218:Myosins