<3110> 人肺动脉平滑肌细胞 （HPASMC）提取于人肺动脉组织，第二代冻存。
 
    平滑肌细胞是多数重要动脉疾病的靶细胞。血管SMC的生长潜力是原发血管病发展中至关重要的异常因素。研究表明SMC表达的钙通道，其表面表达的ICAM-1和VCAM-1，均参与了血管壁的炎症反应，并与血管疾病的进展和稳定有关。慢性肺组织缺氧能造成血管重塑，肺动脉平滑肌增生，zui终导致肺动脉高压。人血管平滑肌的体外培养可作为血管研究模型，为血管疾病的治疗和药理学研究提供信息，发挥重要作用。

    人肺动脉平滑肌细胞 （HPASMC）提取于人肺动脉组织，第二代冻存。每管含有细胞数>5×105 cells/ml，此细胞通过对alpha-SMA和Desmin免疫荧光染色验证，经测试不含有HIV-1、HBV、HCV、支原体、细菌、酵母和真菌。细胞可以达到15倍增。
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储存：液氮

运输：干冰

用途：科研

Smooth muscle cell （SMC） is the cellular substate of most significant arterial disease [1]. The increased growth potential of vascular SMC represents one of the crucial anomalies responsible for the development of essential vascular diseases. New studies demonstrate that SMC express calcium channels [2] and the expression of ICAM-1 and VCAM-1 on SMC may contribute to the inflammatory reaction in the vascular wall and may actively be involved in the progression and stability of vascular disease [3]. Chronic lung hypoxia causes vascular remodeling with pulmonary artery SMC hyperplasia, resulting in pulmonary hypertension [4]. In vitro culture of human vascular SMC as a model of vascular research played a critical role and continues providing information in the pharmacology and the therapy of vascular diseases.

HPASMC from ScienCell Research Laboratories are isolated from human pulmonary artery. HPASMC are cryopreserved at secondary culture after purification and delivered frozen. Each vial contains >5 x 105 cells in 1 ml volume. HPASMC are characterized by immunofluorescent method with antibodies to alpha-smooth muscle actin and desmin. HPASMC are negative for HIV-1, HBV, HCV, mycoplasma, bacteria, yeast and fungi. HPASMC are guaranteed to further expand for 15 population doublings at the conditions provided by ScienCell Research Laboratories.

Reference
[1] Schwartz, S. M., Campbell, G. R., Campbell, J. H. （1986） Replication of smooth muscle cells in vascular disease. Circ. Res. 58:427-444.
[2] Fan, Q. I., Vanderpool, K., Marsh, J. D. （2004） A 27 bp cis-acting sequence is essential for L-type calcium channel alpha（1C） subunit expression in vascular smooth muscle cells. Biochim Biophys Acta. 1577:401-11.
[3] Braun, M., Pietsch, P., Schror, K., Baumann, G., Felix, S. B. （1999） Cellular adhesion molecules on vascular smooth muscle cells. Cardiovasc. Res. 41:395-401.
[4] Rose, F., et al. （2004） Hypoxic pulmonary artery fibroblasts trigger proliferation of vascular smooth muscle cells: role of hypoxia-inducible transcription factors. FASEB J. 12:1660-1.