Cell Applications Human Pulmonary Artery Smooth Muscle Cells: HPASMC

Cell Applications Human Pulmonary Artery Smooth Muscle Cells: HPASMC

人肺动脉平滑肌细胞

Description:

Human Pulmonary Artery Smooth Muscle Cells (HPASMC) from Cell Applications, Inc. have been used to show that:

  • Antitumor drugs can selectively target remodeled pulmonary vessels, but not normal vessels
  • Serotonin induces their growth and activates the BMP receptor
  • IL-22 promotes the growth of pulmonary vascular SMCs via a signaling mechanism that involves NADPH oxidase-dependent oxidation
  • Inducers of pulmonary hypertension, characterized by thickened pulmonary arterial walls, can be suppressed by targeting gene transcription
  • Cell growth can be suppressed by trans-retinoic acid by inducing expression of a known cell growth suppressor,
  • Retinoic acid and its receptors may be involved in cell growth and pulmonary vascular remodeling
  • Iron chelation exerts effects on vascular remodeling and is implicated for development of pulmonary hypertension as a result of ROS activity

Tissue:

Normal human pulmonary artery.  Each lot is tested negative for HIV, Hepatitis B, Hepatitis C, mycoplasma, bacteria, and fungi. 

 

Cryopreserved ampoule:

2nd passage, >500,000 cells in Basal Medium containing 10% FBS & 10% DMSO.

 

Kit contains:

Ampoule of cryopreserved HPASMC (352-05a), 500 ml of Smooth Muscle Cell Media (311-500), and a Subculture Reagent Kit (090K).

 

Population doublings:

Can be cultured at least 16 doublings

 

Publications:

2016
Sahoo, S., D. Meijles, I. Ghouleh, M. Tandon, E. Cifuentes-Pagano, J. Sembrat, M. Rojas, E. Goncharova and P. Pagano. 2016. MEF2C-MYOCD and Leiomodin1 Suppression by miRNA-214 Promotes Smooth Muscle Cell Phenotype Switching in Pulmonary Arterial Hypertension. PLoS ONE, dx.doi.org/10.1371/journal.pone.0153780.
2014
Ibrahim, Y.F., C.M. Wong, L. Pavlickova, L. Liu, L. Trasar, G. Bansal, and Y.J. Suzuki. 2014. Mechanism of the Susceptibility of Remodeled Pulmonary Vessels to Drug‐Induced Cell Killing. J. American Heart Association. 10.1161/jaha.1113.000520.
(完)

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