Human Coronary Artery Smooth Muscle Cells: HCASMC, adult
SIGMA/350-05A
Synonym: HCASMC cells
Product Type: Product-on-demand
Cell Applications : Human Coronary Artery Smooth Muscle Cells, HCASMC
| biological source | human coronary artery (normal, tunica intima and media) |
| growth mode | Adherent |
| karyotype | 2n = 46 |
| manufacturer/tradename | Cell Applications, Inc |
| morphology | smooth muscle |
| packaging | pkg of 500,000 cells |
| Quality Level | 100  |
| relevant disease(s) | diabetes; stroke; cardiovascular diseases |
| shipped in | dry ice |
| storage temp. | −196°C |
| technique(s) | cell culture | mammalian: suitable |
| Application: | vascular research, supply of blood to heart muscle |
| Cell Line Origin: | Artery |
| Components: | Basal Medium containing 10% FBS & 10% DMSO |
| Disclaimer: | RESEARCH USE ONLY. This product is regulated in France when intended to be used for scientific purposes, including for import and export activities (Article L 1211-1 paragraph 2 of the Public Health Code). The purchaser (i.e. enduser) is required to obtain an import authorization from the France Ministry of Research referred in the Article L1245-5-1 II. of Public Health Code. By ordering this product, you are confirming that you have obtained the proper import authorization. |
| General description: | Lot specific orders are not able to be placed through the web. Contact your local sales rep for more details. Human Coronary Artery Smooth Muscle Cells (HCASMC) provide an excellent model system to study all aspects of cardiovascular function and disease, especially those related to mechanisms of hyperplasia and hypertrophy of intimal smooth muscle cells leading to vascular occlusion in atherosclerosis and stent restenosis. HCASMC has been utilized in a number of research studies, for example, to: • Study signaling pathways regulating smooth muscle differentiation (Zhou, 2010); and chronic inflammation of arterial wall that leads to artherosclerosis (Kiyan, 2014) • Demonstrate that STAT-1 and STAT-3 regulate VEGF production in smooth muscle cells by having opposing effects on HIF-1α expression (Albasanz-Puig, 2012); study the mechanisms of hypoxia and reoxigenation injuries in by demonstrating increased production of ROS and inflammatory cytokines, and further showing that DHA is not beneficial in this type of injuries (Feng, 2012) • Investigate the gene expression differences between smooth muscle cells from different arteries, underlying their differential response to injuries and proliferation stimuli (Lange, 2013) • Suggest the hypermethylation of SOCS3 gene as the connection between TNF-α and IGF-1 released in response to mechanical injury during coronary intervention, and the induction of cytokines leading to intimal hyperplasia and restenosis (Dhar, 2013) • Develop a novel VEGFR/MET-targeted inhibitor with improved antitumor efficacy and decreased toxicity (Fujita, 2013); and investigate novel therapies and drug combinations to achieve optimal target selectivity (Lehar, 2009; Wo-Wong, 2013) • Develop elastic scaffolds for tissue engineering (Nivison-Smith, 2010, 2012) and novel treatment strategies to prevent stent restenosis by designing new materials (Crowder, 2012), or drug therapies to preferentially inhibit smooth muscle cell growth (O’Neill, 2009; Mociornita, 2013) Characterization: positive for smooth muscle cell specific alpha-actin expression. |
| Preparation Note: | • 2nd passage, >500,000 cells in Basal Medium containing 10% FBS & 10% DMSO • Can be cultured at least 16 doublings |
| Subculture Routine: | Please refer to the HCASMC Culture Protocol . |
| RIDADR | NONH for all modes of transport |
| WGK Germany | WGK 3 |
| Flash Point(F) | Not applicable |
| Flash Point(C) | Not applicable |
| Storage Temp. | −196°C |
| UNSPSC | 41106514 |