Characterisation of postnatal growth of the murine heart

Citation
M. Leu et al., Characterisation of postnatal growth of the murine heart, ANAT EMBRYO, 204(3), 2001, pp. 217-224
Citations number
33
Categorie Soggetti
Cell & Developmental Biology
Journal title
ANATOMY AND EMBRYOLOGY
ISSN journal
03402061 → ACNP
Volume
204
Issue
3
Year of publication
2001
Pages
217 - 224
Database
ISI
SICI code
0340-2061(200109)204:3<217:COPGOT>2.0.ZU;2-W
Abstract
Using a new technique to isolate rod-shaped cardiomyocytes from small tissu e pieces we were able to, analyse the developmental profile of postnatal ca rdiomyocyte growth in the mouse. During the first 4 postnatal days the volu me of the cardiomyocytes remains relatively constant despite a concomitant increase in heart weight, indicating growth due to cell division of the car diomyocytes, also called hyperplasia. After postnatal day 5 the volume of t he cardiomyocytes increases dramatically until postnatal day 14, when the i ncrement of the volume curve decreases again. The cardiomyocytes reach thei r adult volume at around 3 months of age. These measurements present the fi rst detailed analysis of the phase of so-called developmental hypertrophy, i.e. normal cardiomyocyte growth in the mouse, and provide an essential bas e-line for the analysis of growth parameters in mouse models for cardiomyop athies. We used this method to characterise the growth characteristics of c ardiomyocytes from MLP (muscle LIM protein) knockout mice, a mouse model fo r dilated cardiomyopathy. During the first 2 postnatal weeks there is no si gnificant difference in the growth parameters between MLP knockout and wild type mice. However, in the adult animals cardiomyocytes from MLP knockout m ice are not only characterised by a more irregular shape, but also by a hig h variability in size compared to cardiomyocytes from wildtype animals. Thi s suggests that the alterations in ventricular morphology in the MLP heart are not due to a general elongation of the cardiomyocytes but to myocyte di sarray and ventricular wall thinning caused by the heterogeneous volume of the cardiomyocyte population.