ArticleMolecular and cellular biochemistry1998
Differential expression and localization of annexin V in cardiac myocytes during growth and hypertrophy.
Article in Molecular and cellular biochemistry, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 14 citations in OpenAlex.
- Systematic identification of pathological lamin A interactors.Molecular biology of the cell · 2014Article
- Oxidative stress as a common mediator for apoptosis induced-cardiac damage in diabetic rats.The open cardiovascular medicine journal · 2008Article
- Expression profiling reveals distinct sets of genes altered during induction and regression of cardiac hypertrophy.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
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5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Recently it was shown that annexin V is the most prominent member of the annexin family in the adult heart [1]. Amongst others, annexin V has been suggested to play a role in developmental processes. The aim of the present study was to explore whether in the heart annexin V content and localization change during maturational and hypertrophic growth, in order to obtain indications that annexin V is involved in cardiac growth processes. First, in the intact rat heart annexin V content and localization were studied during perinatal development. It was clearly demonstrated that annexin V content in total heart transiently increased in the first week after birth, from 0.79 +/- 0.06 microg/mg protein at 1 day before birth to a peak value of 1.24 +/- 0.08 microg/mg protein 6 days after birth, whereafter annexin V protein levels declined to a value of 0.70 +/- 0.06 microg/mg protein at 84 days after birth (p < 0.05). Differences in annexin V content were also observed between myocytes isolated from neonatal and adult hearts [0.81 +/- 0.09 and 0.17 +/- 0.08 microg/mg protein, respectively (p < 0.05)]. Moreover, during cardiac maturational growth the subcellular localization of annexin V might change from a cytoplasmic to a more prominent sarcolemmal localization. Second, in vivo hypertrophy induced by aortic coarctation resulted in a marked degree of hypertrophy (22% increase in ventricular weight), but was not associated with a change in annexin V localization or content. The quantitative results obtained with intact hypertrophic rat hearts are supported by findings in neonatal ventricular myocytes, in which hypertrophy was induced by phenylephrine (10(-5) M). In the latter model no changes in annexin V content could be observed either. In conclusion, the marked alterations in annexin V content during the maturational growth in the heart suggest a possible involvement of this protein in this process. In contrast, the absence of changes in annexin V content and localization in hypertrophied hearts compared to age matched control hearts suggests that annexin V does not play a crucial role in the maintenance of the hypertrophic phenotype of the cardiac muscle cell. This notion is supported by observations in phenylephrine-induced hypertrophied neonatal cardiomyocytes.
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