Role of formic receptors in soluble urokinase receptor-induced human vascular smooth muscle migration.

Background: Vascular smooth muscle cell (VSMC) migration in response to urokinase is dependent on binding of the urokinase molecule to the urokinase plasminogen receptor (uPAR) and cleavage of the receptor. The aim of this study was to examine the role of the soluble uPAR (suPAR) in VSMC migration.

Methods: Human VSMCs were cultured in vitro.

Protease-mediated human smooth muscle cell proliferation by urokinase requires epidermal growth factor receptor transactivation by triple membrane signaling.

Background: Urokinase (uPA) modulates cellular and extracellular matrix responses within the microenvironment of the vessel wall and has been shown to activate the epidermal growth factor receptor (EGFR). This study examines the role of the protease domain of uPA during EGFR activation in human vascular smooth muscle cells (VSMC).

Methods: Human coronary VSMC were cultured in vitro.

Effect of metabolic syndrome on the response to arterial injury.

Background: Metabolic syndrome is now an epidemic in the United States population. Intimal hyperplasia remains the principal lesion in the development of restenosis after vessel wall injury. The aim of this study is to characterize the changes induced in wall morphology in the developing intimal hyperplasia within a murine model in the presence of diabetes (type 1) and metabolic syndrome.

Urokinase requires NAD(P)H oxidase to transactivate the epidermal growth factor receptor.

Background: Cell migration is an integral part of the development of intimal hyperplasia, and proteases are pivotal components in the process. Cell migration in response to urokinase is mediated through the aminoterminal fragment (ATF) of the protein. This study examines the role of NAD(P)H oxidase during epidermal growth factor receptor (EGFR) transactivation by ATF in human vascular smooth muscle cells (VSMC).

Role of S-1-P receptors and human vascular smooth muscle cell migration in diabetes and metabolic syndrome.

Background: Sphingosine-1-phosphate (S-1-P) is a bioactive sphingolipid released from activated platelets that stimulates migration of vascular smooth muscle cells (VSMC) in vitro. S-1-P is associated with oxidized low-density lipoprotein (oxLDL) and is important in vessel remodeling. S-1-P will activate multiple G protein-coupled receptors (S-1-PR 1 to 5), which can regulate multiple cellular functions, including cell migration.

SRC regulates sphingosine-1-phosphate mediated smooth muscle cell migration.

Background: Sphingosine-1-phosphate (S-1-P) is a bioactive sphingolipid released from activated platelets at sites of arterial injury that stimulates migration of smooth muscle cells (SMC). The kinase src is a significant focal point in transmembrane signaling. This study examines the role of src during smooth muscle cell migration in response to S-1-P.

Role of IL-10 in the resolution of airway inflammation.

IL-10 can be considered an important agent in the resolution of inflammation. Originally named "cytokine synthesis inhibitory factor" for its ability to inhibit IFN-gamma and IL-2 production in Th2 cells, it is secreted by monocytes, macrophages, mast cells, T and B lymphocytes, and dendritic cells (DCs). IL-10 production and release by monocytic cells in response to allergic challenge is upregulated by TNF-alpha, and by negative feedback regulation of itself.