Description

Smooth muscle cells (SMCs) are key contributors to the progression of arterial diseases. The ability of vascular SMCs to switch to a proliferative phenotype is one of the major drivers underlying the development and advancement of vascular disorders. Pulmonary artery smooth muscle cells (PASMCs) express VEGF and FGF-2, and are subjected to mechanical forces under pulsatile blood flow. Chronic pulmonary hypoxia induces vascular remodeling accompanied by PASMC proliferation, ultimately leading to pulmonary arterial hypertension. Cultured PASMCs play an important role in vascular disease research and can be utilized to identify novel therapeutic targets for the treatment of pulmonary vascular diseases.

Immortalized Human Pulmonary Artery Smooth Muscle Cells were transduced with lentivirus carrying the SV40 gene and puromycin resistance. Tests confirmed that the cells are free from bacterial and fungal contamination, exhibit excellent proliferation potential, and can be passaged 10-20 times in vitro.