Human Pulmonary Artery Smooth Muscle Cells: HPASMC, adult
SIGMA/352-05A
Product Type: Product-on-demand
biological source | human intrathoratic artery (normal) |
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) | cardiovascular diseases |
shipped in | dry ice |
storage temp. | −196°C |
technique(s) | cell culture | mammalian: suitable |
Application: | cell growth, signaling, receptor transactivation and suppression, vascular remodeling |
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. HPASMC has been used to show that IL-22 promotes the growth of pulmonary vascular SMCs via a signaling mechanism that involves NADPH oxidase-dependent oxidation (Bansal, 2013). Inducers of pulmonary hypertension, characterized by thickened pulmonary arterial walls, activate expression of anti-apoptotic Bcl-xL gene via binding of GATA-4 to its promoter; the activation can be suppressed by targeting gata4 gene transcription (Suzuki, 2007). Serotonin induces growth of Pulmonary Artery Smooth Muscle Cells and is able to transactivate the BMP receptor in pulmonary artery SMCs, leading to activation of Smads 1/5/8 via Rho and Rho kinase pathway (Liu, 2009). Pulmonary Artery Smooth Muscle Cells growth can be suppressed by trans-retinoic acid by inducing expression of GADD45A, a known cell growth suppressor, downstream of the retinoid acid receptors RARalpha, RARbeta, RARgamma, RXRalpha, and RXRbeta, indicating possible involvement of retinoic acid in pulmonary vascular remodeling (Preston, 2005). Treatment of Pulmonary Artery Smooth Muscle Cells with plasma containing reduced levels of all-trans RA and 13-cis RA promoted cell growth (Day, 2009). Retinoic acid was also shown to inhibit migration of pulmonary smooth muscle cells by inhibiting PI3K/Akt-dependent reorganization of actin cytoskeleton (Day, 2006). Pulmonary Artery Smooth Muscle Cells were also used to study effects of iron chelation on vascular remodeling and its implications for development of pulmonary hypertension as a result of ROS activity (Wong, 2012). Finally, these cells were used to show that antitumor drugs can selectively target remodeled pulmonary vessels, but not normal vessels (Ibragim, 2014). 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 HPASMC 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 |