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Human aortic, pulmonary artery, lung, and coronary artery smooth muscle cells

Vascular Smooth Muscle Cells and the Latest Research Studies

Vascular smooth muscle cells (VSMCs) line blood vessels, providing a structural foundation and controlling vessel constriction and relaxation, which regulates blood flow and pressure.

Vascular smooth muscle cell contraction is regulated by multiple factors, including mechanical, chemical, and electrical stimuli.

VSMCs are also involved in maintaining the integrity of blood vessels and are key factors in vessel repair following damage.

However, dysregulated VSMC function, including aberrant proliferation, migration, and extracellular matrix remodeling, is associated with vascular diseases, such as atherosclerosis, inflammation, and intimal hyperplasia.

Studies Using Lifeline® Vascular Smooth Muscle Cells

Endothelin-1 (ET-1) is an endothelial cell-derived factor that regulates vascular constriction. High levels of ET-1, however, are associated with increased vascular inflammation. Yang et al. set out to define the downstream factors that mediate ET-1- induced transcription of pro-inflammatory cytokines in vascular smooth muscle cells. They found that myocardin-related transcription factor A (MRTF-A) is required for the transcription of IL-6, IL-1, MCP-1, and TNF-a downstream of ET-1. Furthermore, they reported that MRTF-A is central to an epigenetic complex that includes ASH2, BRG1, and BRM, and mediates pro-inflammatory gene transcription in response to ET-1. The authors used LifeLine® human primary aortic smooth muscle cells (HASMCs) grown in VascuLife® medium to study the epigenetic regulation of the ET-1-induced pro-inflammatory response.

Arnold et al. evaluated the efficiency of multiple transfection methods for potential use in gene therapy for vascular disease. The authors used Santa Cruz and DharmaFECT chemical transfection reagents, and the StemFECT bioconjugate polymer reagent to compare the delivery of siRNA against the housekeeping gene, GAPDH. They found that the StemFECT polymeric transfection method resulted in the most efficient GAPDH knockdown in LifeLine® human primary aortic smooth muscle cells (HASMCs) grown in VascuLife® medium. Their results suggest that polymeric transfection methods may hold promise for gene therapy strategies.

Intimal hyperplasia can occur following a bypass graft and has been reported to occur more often in postmenopausal women taking hormone replacement therapy compared with those not taking hormone replacement therapy. Mountain et al. investigated the mechanism by which estrogen treatment of vascular smooth muscle cells might result in increased incidence of intimal hyperplasia. They previously identified that estrogen increases matrix metalloproteinase 2 (MMP2) activity, which is associated with development of intimal hyperplasia. Here, they found that silencing of membrane type-matrix metalloproteinase 1 (MT1-MMP)—an MMP2 activator—resulted in decreased vascular smooth muscle cell proliferation in response to estrogen treatment, with no effects on cell migration or invasion. Their results implicate MT1-MMP in estrogen-induced cell proliferation, but suggest there are other factors involved. The authors used LifeLine® human primary aortic smooth muscle cells (HASMCs) from a 61-year-old female donor grown in in VascuLife® medium.

 Lifeline® Vascular Smooth Muscle Cells

Lifeline® vascular smooth muscle cells can be used to study:

  • Normal vascular physiology
  • VSMC proliferation, migration, and invasion
  • Vascular disease
  • Therapeutic strategies targeting vascular diseases

Lifeline® offers various vascular smooth muscle cells from different primary locations including:

For optimal vascular smooth muscle cell growth, Lifeline® offers VascuLife® SMC Medium.

Tell us how you are using Lifeline® cells to answer your research questions, and your study could be featured on our blog!

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