Human Intestinal Smooth Muscle Cells (HISMC)

Product Description

Smooth muscle contraction is the fundamental event in gastrointestinal motion. Although many of the biochemical mechanisms underlying the excitation-contraction coupling are not yet defined, it is known that cytosolic Ca2+ is the essential component in the coupling phenomenon. Inflammation of the human intestine causes increased levels of smooth muscle-specific actin, which in turn promotes the thickening of the smooth muscle layers. The increased smooth muscle actin may affect force production and further demonstrates the plasticity of smooth muscle cells in the inflamed intestine ^[1]. Studies also show that human intestinal smooth muscle cells (HISMC) respond to IL-1beta and TNF-alpha stimulation by releasing IL-6, which may significantly contribute to the overall systemic inflammatory response ^[2]. The availability of HISMC makes it more feasible to study the contractile and proliferative tissue responses of human intestinal smooth muscle.

iXCells Biotechnologies provides high quality Human Intestinal Smooth Muscle Cells (HISMC), which are isolated from human bronchi and bronchioles and cryopreserved at P1, with ≥ 0.5 million cells in each vial. HISMC express α-smooth muscle actin and desmin and are negative for HIV-1, HBV, HCV, mycoplasma, bacteria, yeast, and fungi. HISMC can further expand for no more than 3 passages in Smooth Muscle Cell Growth Medium (Cat # MD-0034) under the condition suggested by iXCells Biotechnologies.

Figure 1. Human Intestinal Smooth Muscle Cells (HISMC). (A) Phase contrast image of HISMC; (B) ICC image using α-SMA antibody.

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References

[1]. Blennerhassett, M. G., Bovell, F. M., Lourenssen, S., McHugh, K. M. (1999) Characteristics of inflammation-induced hypertrophy of rat intestinal smooth muscle cell. Dig Dis Sci. 44(7):1265-72.

[2]. Ng, E. K., Panesar, N., Longo, W. E., Shapiro, M. J., Kaminski, D. L., Tolman, K. C., Mazuski, J. E. (2003) Human intestinal smooth muscle cells are potent producers of IL-6. Mediators Inflamm. 12(1):3-8.

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