The 60S ribosomal subunit co-localizes with myofibrils in spreading cardiac myocytes, suggesting a role for ribosomes in the maintenance and growth of the contractile apparatus during cellular remodeling.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications for hypertrophy; leaves open ribosomal roles in myofibril dynamics and requires in vivo validation.
Cardiac myocytes in culture undergo considerable structural reorganization. The remodeling of the myofibrils and the nonmyofibrillar cytoskeleton that occurs in the spreading cardiac myocytes resembles the cellular features observed in the hypertrophying heart. In this study we examined the distribution of the large 60S ribosomal subunit in freshly isolated cardiac myocytes and during the course of attachment and spreading in culture. Initially, anti-60S immunolabeling was scattered widely throughout the sarcoplasm of the dissociated cardiac myocytes. After attachment to the substrate, the 60S ribosomal subunit attained wide sarcoplasmic localization before a sarcomere-related staining pattern appeared in the spreading cell. Double labeling experiments with alpha-actinin confirmed co-localization of the 60S ribosomal subunit with nascent and mature myofibrils. These findings demonstrate that translocation of the 60S ribosomal subunit coincides with the cytoskeletal reorganization taking place in these cells. Moreover, the close association between the myofibrils indicates a particular role for the ribosomes in maintenance and growth of the contractile apparatus. (J Histochem Cytochem 46:963-969, 1998)
No takes yet. Share an insight, caveat, or question.
Larsen et al. (1998) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: