What is smooth muscle proliferation?

Proliferation of smooth muscle cells (SMCs) represents an important event in vascular lesion formation. The results of this study support the concept that endogenous bFGF is the major mitogen controlling the growth of vascular smooth muscle cells following injury.

What causes smooth muscle cell proliferation?

After injury, there is deposition of platelets that release platelet-derived growth factor (PDGF) and other mitogenic factors that penetrate the vascular wall and trigger medial vascular smooth muscle cell proliferation and migration. The platelets also release chemokines, which initiate an inflammatory response.

Can smooth muscle cells proliferate?

Vascular smooth muscle cell (VSMC) proliferation is an important component of vessel wall remodelling in response to injury, for example, after angioplasty or vein grafting, and during atherosclerosis formation.

What is smooth muscle migration?

Smooth muscle cell migration occurs during vascular development, in response to vascular injury, and during atherogenesis. Actin filament remodeling, focal contact remodeling, and molecular motors are coordinated to cause cells to migrate along gradients of chemical cues, matrix adhesiveness, or matrix stiffness.

What kind of membrane does ADAM17 come from?

ADAM17 has been purified from human monocytic cell plasma membranes [1] and pig spleen microsomal membranes [3].

What was the purpose of the discovery of ADAM17?

ADAM17 was first discovered in a search for molecules that regulate the release of the potent pro-inflammatory cytokine tumor necrosis factor α (TNFα) (Black et al., 1997; Moss et al., 1997 ).

How is ADAM17 related to skin and bowel disease?

Genetic deficiency of ADAM17 has been linked to neonatal inflammatory skin and bowel disease, yet the pathogenic mechanisms remained unclear, particularly given the number of potential substrates that this protease can cleave.

Why are mice born without the ADAM17 gene?

Mice lacking ADAM17 are born with respiratory distress, presumably caused by abnormal alveoli with septation defects and thickened mesenchyme as well as impaired branching morphogenesis and delayed vasculogenesis, and thus reduced surface for gas exchange.