心肌细胞是机体上有活力的细胞。它的收缩是肌源性的，其活动与神经刺激无关。所有的心肌细胞都能自发的、有节律的进行细胞膜的去极化和复极化。心肌细胞占有心脏重量的75%，约为心脏细胞数量的1/3。它们是具有高氧含量及含有大量线粒体的一类细胞。分化的心肌细胞几乎无增生能力，在肾上腺素经过Ras/MEK途径的刺激下，细胞表现为肥大。心力衰竭时心肌细胞肥大和凋亡时心脏的收缩功能下降。心肌细胞有着复杂的信号网络，调控心脏泵功能的节律性。该信号网络是研究心肌细胞死亡的细胞信号调控机理的有效模型。

    大鼠心肌细胞（RCM）提取于大鼠心脏组织，原代冻存。每管含有细胞数>1×106cells/ml，此细胞通过对Myosin免疫荧光染色验证，经测试不含有支原体、细菌、酵母和真菌。
*培养基:上海沪峰生物科技有限公司

储存：液氮

运输：干冰

用途：科研

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.

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