Rat Cardiac Myocytes
(RCM)

Catalog # R6200
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Description

The cardiac myocyte is the most physically energetic cell in the body. Its contraction is myogenic, i.e. it is independent of nervous stimulation. All cardiac myocyte are capable of spontaneous rhythmic depolarization and repolarization of their membrane. Cardiac myocytes occupy as much as 75% of cardiac mass but constitute only about one third of the total cell number in the heart. They are highly specialized high-oxygen-content cells and house a large number of mitochondria [1]. Differentiated cardiac myocytes have little capacity to proliferate and show the hypertrophic growth in response to alpha1-adrenergic stimuli via the Ras/MEK pathway [2]. Cardiac myocyte hypertrophy and apoptosis have been implicated in the loss of contractile function during heart failure. Cardiac myocytes have a complex network of signals that regulates their essential role in the rhythmic pumping of the heart [3]. This network is an appealing model system in which to study the basic principles of cellular signaling mechanisms leading to cardiac myocyte death.

RCM from ScienCell Research Laboratories are isolated from rat heart. RCM are cryopreserved on primary cultures and delivered frozen. Each vial contains >1 x 106 cells in 1 ml volume. RCM are characterized by immunofluorescent method with antibody to myosin. RCM are negative for mycoplasma, bacteria, yeast and fungi. RCM are guaranteed to further culture at the condition provided by ScienCell Research Laboratories.

Recommended Medium

It is recommended to use Cardiac Myocyte Medium (CMM, Cat. No. 6201) for the culturing of RCM in vitro.

Product Use

RCM are for research use only. It is not approved for human or animal use, or for application in in vitro diagnostic procedures.

Storage

Directly and immediately transfer cells from dry ice to liquid nitrogen upon receiving and keep the cells in liquid nitrogen until cell culture needed for experiments.

Shipping

Dry ice.

Reference

[1] Bodyak, N., Kang, P. M., Hiromura, M., Sulijoadikusumo, I., Horikoshi, N., Khrapko, K. and Usheva, A. (2004) 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. (2004) 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. (2004) Navigating the signaling network in mouse cardiac myocytes. Nature 420(6916):712-4.