Cardiac myocytes are the most physically energetic cells in the body. They are highly specialized high-oxygen-content cells that house a large number of mitochondria [1]. They occupy as much as 75% of the cardiac mass, but constitute only about one third of the total cell number in the heart. Differentiated cardiac myocytes have little capacity to proliferate; however, hypertrophic growth has been shown to respond to alpha1-adrenergic stimuli via the Ras/MEK pathway [2]. All cardiac myocytes are capable of spontaneous rhythmic depolarization and repolarization of their membranes. Contraction of cardiac myocytes is myogenic, which is independent of nervous stimulation. There is a complex network of signals in cardiac myocytes regulating the rhythmic pumping of the heart [3]. Cardiac myocyte hypertrophy and apoptosis have been implicated in the loss of contractile function during heart failure. A better understanding of the cardiac signaling network will help reveal the cellular mechanisms leading to cardiac myocyte death.
Recommended Medium
It is recommended to use Cardiac Myocyte Medium-serum free (CMM, Cat. No. SC6101) for culturing RCM in vitro.
Product Use
This product is for research use only. It is not approved for use in humans, animals, or in vitro diagnostic procedures.
Storage
Upon receiving, directly and immediately transfer the cells from dry ice to liquid nitrogen and keep the cells in liquid nitrogen until they are needed for experiments.
Shipping
Dry ice
Warranty
Cells are only warranted if ScienCell media and reagents are used and the recommended protocols are followed.
References
[1] Bodyak, N., Kang, P. M., Hiromura, M., Sulijoadikusumo, I., Horikoshi, N., Khrapko, K. and Usheva, A. (2002) Gene expression profiling of the aging mouse cardiac myocytes. Nucleic Acids Research 30(17):3788-3794.
[2] Tamamori-Adachi, M., Ito, H., Nobori, K., Hayashida, K., Kawauchi, J., Adachi, S., Ikeda, M. A. and Kitajima, S. (2002) Expression of cyclin D1 and CDK4 causes hypertrophic growth of cardiomyocytes in culture: a possible implication for cardiac hypertrophy. Biochem Biophys Res Commun 296(2):274-80.
[3] Sambrano, G.R., Fraser, I., Han, H., Ni, Y., O'Connell, T., Yan, Z. and Stull, J. T. (2002) Navigating the signaling network in mouse cardiac myocytes. Nature 420(6916):712-4.