Smooth Muscle Cell Studies: The Force Behind Contraction
Smooth muscle cells (SMCs) reside in the outer layers of blood vessels and other contractile organs, including the bladder, uterus, respiratory tract, and gastrointestinal tract. SMCs contract involuntarily, and molecular motors such as myosin, and the actin cytoskeleton, drive this contraction. This contraction pushes blood through blood vessels, food through the digestive system, and urine from the bladder.
In vitro, SMCs can be used to generate blood vessel-like structures using tissue-engineering applications. In addition, they contract in response to various stimuli, providing an excellent model to study contractility.
Lifeline® provides a number of Smooth muscle cell types, perfect for a wide range of research applications. SMCs are available from the following tissue sites:
All Smooth muscle cell types are optimally grown in VascuLife SMC® medium. Lifeline® SMCs can be used to study cardiovascular disease, pulmonary function, and angiogenesis. The research studies below highlight Lifeline® aortic and bladder SMCs.
Recent Studies Using Lifeline® Aortic and Bladder Smooth Muscle Cells
Vascular grafts are a common treatment option for many conditions, including congenital heart disease. A patient’s own blood vessels can be harvested for grafts, but this process becomes difficult if there are a limiting number of healthy blood vessels, or in the case of congenital heart disease, the patient is simply too small. Tissue-engineered vascular grafts (TEVGs) are a solution to this clinical challenge. TEVGs are generated using a biodegradable polymer scaffold on which smooth muscle cells (SMCs) and endothelial cells from a patient are plated. Following a specific culturing period, these cells will grow together and form a vessel structure that can be introduced into the patient; the scaffold eventually degrades and the blood vessel is left behind. Ye et al. investigated the viability of a TEVG scaffold they developed using electrospinning, a method by which polymer is spun into nanoscale fibers using an electric field. They found that SMCs and endothelial cells seeded on this electrospun polymer scaffold formed a 3D structure that resembled a vessel, with endothelial cells arranged along the lumen and the SMCs along and in the scaffold wall.
The researchers used Lifeline® aortic SMCs in their studies, illustrating that these cells can be used in tissue-engineering applications to build neovessels. Their study demonstrates that this electrospun polymer scaffold is a promising development in the field of TEVG.
Proper bladder function depends on muscle contractions that cause bladder emptying, called detrusor contractility. The stability of the actin cytoskeleton is critical to this contractile response, and injury to the cytoskeleton can result in incomplete or inadequate contractility, resulting in failure to completely empty the bladder. Wang et al. set out to investigate the role of cytoskeletal modulators to further define the molecular mechanism underlying detrusor contractility. In particular, they focused on heat shock protein 27 (HSP27), which has been implicated as a key mediator between sensing cellular stress and maintenance of the actin cytoskeleton.
The researchers used Lifeline® bladder SMCs throughout their study, and induced cellular stress by plating bladder SMCs on flexible dishes and applying stretch through a vacuum apparatus. They found that HSP27 knockdown caused significant disorganization of the actin cytoskeleton following stretching that did not recover over time. Additionally, cells displayed a lower contractile force than control cells, and a decreased F (filamentous)/G (free monomer)-actin ratio, suggesting that HSP27 function is important for maintaining the structure and integrity of the actin cytoskeleton in response to mechanical stress. In addition, the decreased F/G-actin ratio following HSP27 knockdown suggests that HSP27 might maintain the actin cytoskeleton by preventing depolymerization of actin filaments (F-actin), or inducing polymerization of free actin monomers (G-actin). Together, their results provide a molecular mechanism for the cellular response to mechanical stretch, linking stress response pathways (HSP27) to the actin cytoskeleton.
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