The differential effect of contrast agents on endothelial cell and smooth muscle cell growth in vitro

Sawmiller, Carol J.; Powell, Richard J.; Quader, Mohammed; Dudrick, Stanley J.; Sumpio, Bauer E.

doi:10.1016/s0741-5214(98)70015-1

Cited by 17 publications

(8 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous work reported that brief, high-concentration CM exposure causes injury to endothelial cells and retards their subsequent growth[10,29–31]. In the present study, we demonstrate that prolonged exposure to clinically relevant, low concentrations of CM inhibits the proliferation of endothelial cells.…”

Section: Discussionsupporting

confidence: 73%

Heme oxygenase-1 counteracts contrast media-induced endothelial cell dysfunction

Chang

Liu

Peyton

et al. 2014

Biochemical Pharmacology

View full text Add to dashboard Cite

Endothelial cell (EC) dysfunction is involved in the pathogenesis of contrast-induced acute kidney injury, which is a major adverse event following coronary angiography. In this study, we evaluated the effect of contrast media (CM) on human EC proliferation, migration, and inflammation, and determined if heme oxygenase-1 (HO-1) influences the biological actions of CM. We found that three distinct CM, including high-osmolar (diatrizoate), low-osmolar (iopamidol), and iso-osmolar (iodixanol), stimulated the expression of HO-1 protein and mRNA. The induction of HO-1 was associated with an increase in NF-E2-related factor-2 (Nrf2) activity and reactive oxygen species (ROS). CM also stimulated HO-1 promoter activity and this was prevented by mutating the antioxidant responsive element or by overexpressing dominant-negative Nrf2. In addition, the CM-mediated induction of HO-1 and activation of Nrf2 was abolished by acetylcysteine. Finally, CM inhibited the proliferation and migration of ECs and stimulated the expression of intercellular adhesion molecule-1 and the adhesion of monocytes on ECs. Inhibition or silencing of HO-1 exacerbated the anti-proliferative and inflammatory actions of CM but had no effect on the anti-migratory effect. Thus, induction of HO-1 via the ROS-Nrf2 pathway counteracts the anti-proliferative and inflammatory actions of CM. Therapeutic approaches targeting HO-1 may provide a novel approach in preventing CM-induced endothelial and organ dysfunction.

show abstract

Section: Discussionsupporting

confidence: 73%

Heme oxygenase-1 counteracts contrast media-induced endothelial cell dysfunction

Chang

Liu

Peyton

et al. 2014

Biochemical Pharmacology

View full text Add to dashboard Cite

show abstract

“…However, prior studies suggest that sodium ions, as opposed to osmolality, are the more likely cause. 22,23 Increasing the physiologic sodium ion concentration by 25% reduced vascular SMC numbers by almost 50%. 22 While the chloride concentration also is increased by the addition of NaCl, it too appears unlikely to decrease the number of SMCs.…”

Section: Discussionmentioning

confidence: 99%

Effects of polyglycolic acid on porcine smooth muscle cell growth and differentiation

Higgins

Solan

Niklason

2003

J Biomedical Materials Res

125

View full text Add to dashboard Cite

Polyglycolic acid (PGA) is commonly used as a scaffold for tissue engineering. Recent studies utilized PGA as a scaffold for vascular tissue engineering using bovine and porcine smooth muscle cells (SMCs). In engineered vessels, the SMCs displayed high rates of mitosis and dedifferentiation in areas where PGA fragments were present. We hypothesized that PGA breakdown products, sequestered within a SMC vessel at the conclusion of culture, led to increased proliferation and dedifferentiation of vascular SMCs. To test this hypothesis, the current study assessed possible means by which PGA breakdown products could lead to changes in SMC phenotype. SMCs grown in high concentrations of PGA breakdown products showed, by Western blotting, decreased expression of calponin, a marker for SMC differentiation. The same was true for SMCs grown in glycolic acid (GA), which also showed decreased expression of proliferating cell nuclear antigen (PCNA), a marker for SMC proliferation. In contrast, cells grown in varying amounts of NaCl or HCl showed little change in differentiation. We conclude that, independent of acidity or osmolality, plausible products of PGA degradation appear to induce dedifferentiation of porcine SMCs in vitro. Because of dedifferentiation and decreased mitosis, commercially available PGA may not represent an optimal scaffold for vascular tissue engineering.

show abstract

“…1-3). VSMCs as well as endothelial cells exhibit diminished viability or proliferation in a dose-and time-dependent manner after exposure to CMs in vitro (12,25,31). Intravascular injection of CMs seems to cause adverse effects on the blood vessel, which is composed of endothelial cells and VSMCs.…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, there is less nephrotoxicity with iso-osmolar CMs than with low-osmolar CMs (1). CMs are cytotoxic to the proliferation and the function of endothelial cells and vascular smooth muscle cells (VSMCs) (25,26). Exposure of endothelial cells to CMs induces apoptotic cell death (23) and alters the adhesion of neutrophils (33).…”

mentioning

confidence: 99%

Effect of contrast media on vascular smooth muscle cells

Takatsuki

Furukawa²,

Liu³

et al. 2004

Acta Radiol

View full text Add to dashboard Cite

show abstract

The differential effect of contrast agents on endothelial cell and smooth muscle cell growth in vitro

Cited by 17 publications

References 23 publications

Heme oxygenase-1 counteracts contrast media-induced endothelial cell dysfunction

Heme oxygenase-1 counteracts contrast media-induced endothelial cell dysfunction

Effects of polyglycolic acid on porcine smooth muscle cell growth and differentiation

Effect of contrast media on vascular smooth muscle cells

Contact Info

Product

Resources

About