The Nitric Oxide Precursorl-Arginine Reduces Expression of Hyaluronan Synthase in Experimental Vein Bypass Grafts

Dattilo, Jeffery B.; Dattilo, Mary Peace M.; Crane, Joseph T.; Yager, Dorne R.; Makhoul, Raymond G.

doi:10.1006/jsre.1997.5224

Cited by 6 publications

(2 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…50 L-arginine, the substrate for NO production, significantly diminished hyaluronan synthase expression (one of the two enzymes responsible for making hyaluronan, a key component of the ECM). 51 Another NO donor, DETA/NO, caused cell cycle arrest associated with overexpression of TGF␤-1 and an increase in synthesis of collagen I and III in human coronary VSMC. 52 Conversely, studies have demonstrated inhibition of collagen levels with NO.…”

Section: Effects Of Nitric Oxide On Neointimal Hyperplasiamentioning

confidence: 99%

The role of nitric oxide in the pathophysiology of intimal hyperplasia

Ahanchi

Tsihlis

Kibbe

2007

Journal of Vascular Surgery

View full text Add to dashboard Cite

Since its discovery, nitric oxide (NO) has emerged as a biologically important molecule and was even named Molecule of the Year by Science magazine in 1992. Specific to our interests, NO has been implicated in the regulation of vascular pathology. This review begins with a summary of the molecular biology of NO, from its discovery to the mechanisms of endogenous production. Next, we turn our attention to describing the arterial injury response of neointimal hyperplasia, and we review the role of NO in the pathophysiology of neointimal hyperplasia. Finally, we review the literature regarding NO-based therapies. This includes the development of inhalational-based NO therapies, systemically administered L-arginine and NO donors, NO synthase gene therapy, locally applied NO donors, and NO-releasing prosthetic materials. By reviewing the current literature, we emphasize the tremendous clinical potential that NO-based therapies can have on the development of neointimal hyperplasia.

show abstract

Section: Effects Of Nitric Oxide On Neointimal Hyperplasiamentioning

confidence: 99%

The role of nitric oxide in the pathophysiology of intimal hyperplasia

Ahanchi

Tsihlis

Kibbe

2007

Journal of Vascular Surgery

View full text Add to dashboard Cite

show abstract

“…fMLP has been shown to bind to two different G protein-coupled receptors FPR) and the low affinity FPRL1 to initiate a signal transduction cascade leading to cell activation and migration. In fibroblasts, fMLP requires Gαi coupled, protein kinase C (PKC) and phosphatidylinositol 3-kinase (PI3-K) activation to induce intracellular calcium flux and a transient increase in F-actin in order to facilitate cell migration (17, 18). fMLP also can induce MAPK activation through Gαi2 G-proteins in these cells (19, 20).…”

Section: Discussionmentioning

confidence: 99%

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

Duru

2015

Journal of Surgical Research

View full text Add to dashboard Cite

Background Vascular smooth muscle cell (VSMC) migration in response to urokinase is dependent on binding of the urokinase molecule to the urokinase receptor uPAR and cleavage of the receptor. The aim of this study is to examine the role of the soluble uPAR (suPAR) in vascular smooth muscle cell migration. Methods Human VSMCs were cultured in vitro. Linear wound and Boyden microchemotaxis assays of migration were performed in the presence of suPAR. Inhibitors to G-protein signaling and kinase activation were employed to study these pathways. Assays were performed for MAPK and EGFR activation. Results suPAR induced concentration-dependent migration of VSMC, which was G protein-dependent and was blocked by Gαi and Gβγ inhibitors. Removal of the full uPAR molecule by incubation of the cells with a phospholipase did not interfere with this response. suPAR induced ERK1/2, p38MAPK and JNK activation in a Gαi/Gβγ-dependent manner and interruption of these signaling pathways prevented suPAR-mediated migration. suPAR activity was independent of plasmin activity. suPAR did not activate EGFR. Interruption of the low affinity N-formyl-Met-Leu-Phe receptor (FPRL1) but not high affinity N-formyl-Met-Leu-Phe receptor (FPR) prevented cell migration and activation in response to suPAR. suPAR increased MMP-2 expression and activity, and this was dependent on the low affinity N-formyl-Met-Leu-Phe receptor (FPRL1) and ERK1/2. Conclusion suPAR induces human smooth muscle cell activation and migration independent of the full uPAR through activation of the G protein-coupled receptor FPRL1 which is not linked to the plasminogen activation cascade.

show abstract

Overexpression of hyaluronan synthases alters vascular smooth muscle cell phenotype and promotes monocyte adhesion

Wilkinson¹,

Bressler²,

Evanko³

et al. 2005

Journal Cellular Physiology

View full text Add to dashboard Cite

Hyaluronan (HA) accumulates in vascular disease but its functional role is not fully understood. To investigate the impact of HA enriched extracellular matrices (ECM) on cell phenotype, arterial smooth muscle cells (ASMCs) were transduced with retroviral constructs (LXSN) encoding murine has-1, has-2, and has-3. HA synthesis was significantly elevated in has transduced ASMCs. Metabolically labeled HA from has-1 and has-2 transduced cells was present mostly in high molecular weight (HWA) fractions (2-10x10(6) Da), whereas HA produced by has-3 and control cells was present in lower molecular weight fractions (approximately 2x10(6) Da). Both has-1 and has-3 transduced ASMCs accumulated more pericellular HA than has-2 transduced ASMCs. All has transduced ASMCs had attenuated growth and migration rates, and a decreased detachment response. Affinity histochemistry revealed that has-1 transduced ASMCs accumulated the greatest amount of HA containing ECM than the other transduced ASMCs. This ECM was hyaluronidase sensitive and bound a significantly greater number of monocytes than the ECM generated by has-2 or has-3 transduced ASMCs. Confocal microscopy showed CD44 positive monocytes bound to hyaluronidase sensitive ECM in has-1 transduced ASMCs. These data implicate specific has isoforms in the formation of HA enriched pro-inflammatory ECMs.

show abstract

The Nitric Oxide Precursorl-Arginine Reduces Expression of Hyaluronan Synthase in Experimental Vein Bypass Grafts

Cited by 6 publications

References 10 publications

The role of nitric oxide in the pathophysiology of intimal hyperplasia

The role of nitric oxide in the pathophysiology of intimal hyperplasia

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

Overexpression of hyaluronan synthases alters vascular smooth muscle cell phenotype and promotes monocyte adhesion

Contact Info

Product

Resources

About