Differential expression and localization of annexin V in cardiac myocytes during growth and hypertrophy.
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.
Jans
S W
SW
Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, The Netherlands.
de Jong
Y F
YF
Reutelingsperger
C P
CP
van der Vusse
G J
GJ
van Bilsen
M
M
D000818:Animals; D017304:Annexin A5 / Q000096:biosynthesis*; D006332:Cardiomegaly / Q000378:metabolism*; D002316:Cardiotonic Agents / Q000494:pharmacology; D002454:Cell Differentiation; D005260:Female; D006321:Heart / Q000254:growth & development*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010656:Phenylephrine / Q000494:pharmacology; D011247:Pregnancy; D051381:Rats; D011917:Rats, Inbred Lew; D011921:Rats, Inbred WKY
D017304:Annexin A5; D002316:Cardiotonic Agents; D010656:Phenylephrine