Cardiac hypertrophy cannot proceed without initial suppression of protein synthesis.
Stress was induced in rat hearts by heat shock and aortic banding and in cardiac cell cultures by heat shock. Proteins were labeled with [35S]-methionine, resolved by electrophoresis, and isotope incorporation measured. Determinations were made during and following stress. The immediate response was stress protein (SP) synthesis, cessation of normally occurring protein synthesis and reduced isotope incorporation. Following recovery, the prestress protein pattern returned, SP synthesis remained high and label incorporation doubled. Response of hearts to the two stresses were similar. Initial suppression may be an important precursor to accelerated protein synthesis seen in hypertrophy.
D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism*; D006360:Heat-Shock Proteins / Q000096:biosynthesis*; D009124:Muscle Proteins / Q000096:biosynthesis*; D051381:Rats; D013312:Stress, Physiological / Q000378:metabolism; D014655:Vascular Resistance
D006360:Heat-Shock Proteins; D009124:Muscle Proteins