Neonatal rat cardiomyocytes possess a large population of stable microtubules that is enriched in post-translationally modified subunits.
Neonatal rat cardiomyocytes possess a large population of stable microtubules that is enriched in post-translationally modified subunits.
复制标题
新生大鼠心肌细胞拥有大量稳定的微管,这些微管富含翻译后修饰的亚基。
DOI:
10.1006/jmcc.1997.0517
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发表时间:
1997
影响因子:
5
通讯作者:
D. Webster
中科院分区:
文献类型:
--
作者:
D. Webster
Microtubules (MTs) may be involved in several differentiation-specific cardiomyocyte functions, including myofibril organization, hypertrophic cell growth, and the negative regulation of heart cell contraction. The functional characteristics of neonatal rat heart cell MTs, which possess subsets that are enriched with either detyrosinated or acetylated tubulin subunits, were analysed. When compared with their non-myocyte neighbors, cardiomyocyte MTs were found to be more resistant to high concentrations (33 microM) of nocodazole (over 10-30 min), cold treatments (10 min to 8 h), or calcium (50-100 microM for 1-10 min, using detergent-extracted cells). These stable MTs were correlated with the modified MT population. Myocytes treated with 10 microM taxol for 4 h showed elevated levels of modified tubulin but only moderate MT bundling or rearrangement, while after an overnight treatment significant changes in intensity and distribution were noted. In contrast, non-myocytes on the same coverslip showed much greater MT rearrangements, but with only a moderate increase in the immunostaining intensity for modified MTs. Finally, hapten-labeled tubulin that was microinjected into the myocytes showed incorporation rates that were similar to those of the non-myocytes in this study as well as to fibroblast rates determined in other studies, suggesting that the modified MTs in cardiomyocytes may be only moderately stable. Thus, a significant subset of MTs in neonatal cardiomyocytes are post-translationally modified, are resistant to depolymerization by a variety of agents, but are still turning over. These MTs may help define myocyte function during heart development.