Effect of vascular stent alloys on expression of cellular adhesion molecules by endothelial cells

Regina L W Messer, John C. Wataha, Jill B. Lewis, Petra E. Lockwood, Gretchen B Caughman, Wu Yan Tseng

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Objective. Nickel and cobalt ions activate ICAM1 expression on endothelial cells and keratinocytes. Furthermore, these ions are released in vitro and in vivo from the types of alloys used for vascular stents, but the full biological consequences of this release is not known. In the current study, we determined if release of elements from vascular stent alloys that contained nickel and cobalt was sufficient to activate expression of key cellular adhesion molecules (CAMs) by endothelial cells. Expression of these CAMs is a critical step in the long-term inflammatory response to stent materials and possibly to in-stent restenonsis. Methods. Stainless steel, NiTi, CoCrNi, and NiCr alloys were placed in direct contact with primary human microvascular endothelial cells for 72 hours after preparation at three roughnesses (120, 320, and 1200 grit). Expression of three CAMs-ICAM1, VCAM1, and e-selectin-was assessed using a modified ELISA procedure. Cytotoxicity of the alloys was assessed by measuring succinate dehydrogenase (SDH) activity and total protein content of the cells, and nickel release was measured by atomic absorption spectroscopy. Results. None of the alloys suppressed SDH activity or total cellular protein significantly at any surface roughness, indicating little or no cytotoxicity. Ni release was measurable from all alloys, was greatest from the rougher surfaces, and was significantly different for the different alloy types. NiTi alloys exhibited the lowest nickel release. However, none of the alloys activated expression of the CAMs, regardless of surface roughness or nickel release level; Supplemental experiments using nickel ions alone confirmed that ICAM1 was inducible on the endothelial cells by Ni(II) concentrations above 100 μM. Conclusions. In this in vitro system, nickel or other elemental release from several common types of stent alloys was not sufficient to activate expression of CAMs on endothelial surfaces. Although these results indicate a low risk for direct activation of endothelial cells by ions released from stent alloys, other mechanisms, such as modulation of CAM expression by monocytes or smooth muscle cells, must be considered before ion-mediated influence on CAM expression can be dismissed.

Original languageEnglish (US)
Pages (from-to)39-47
Number of pages9
JournalJournal of Long-Term Effects of Medical Implants
Volume15
Issue number1
DOIs
StatePublished - Feb 22 2005

Fingerprint

Stents
Endothelial cells
Blood Vessels
Adhesion
Endothelial Cells
Nickel
Molecules
Ions
Succinate Dehydrogenase
Surface roughness
Cytotoxicity
Cobalt
Proteins
Selectins
Atomic spectroscopy
Stainless Steel
Absorption spectroscopy
Keratinocytes
Smooth Muscle Myocytes
Muscle

Keywords

  • Atherosclerosis
  • Biocompatibility
  • Cobalt
  • E-selectin
  • ICAM1
  • Monocytes
  • Nickel
  • Restenosis
  • VCAM1

ASJC Scopus subject areas

  • Biomedical Engineering
  • Dentistry(all)

Cite this

Effect of vascular stent alloys on expression of cellular adhesion molecules by endothelial cells. / Messer, Regina L W; Wataha, John C.; Lewis, Jill B.; Lockwood, Petra E.; Caughman, Gretchen B; Tseng, Wu Yan.

In: Journal of Long-Term Effects of Medical Implants, Vol. 15, No. 1, 22.02.2005, p. 39-47.

Research output: Contribution to journalArticle

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abstract = "Objective. Nickel and cobalt ions activate ICAM1 expression on endothelial cells and keratinocytes. Furthermore, these ions are released in vitro and in vivo from the types of alloys used for vascular stents, but the full biological consequences of this release is not known. In the current study, we determined if release of elements from vascular stent alloys that contained nickel and cobalt was sufficient to activate expression of key cellular adhesion molecules (CAMs) by endothelial cells. Expression of these CAMs is a critical step in the long-term inflammatory response to stent materials and possibly to in-stent restenonsis. Methods. Stainless steel, NiTi, CoCrNi, and NiCr alloys were placed in direct contact with primary human microvascular endothelial cells for 72 hours after preparation at three roughnesses (120, 320, and 1200 grit). Expression of three CAMs-ICAM1, VCAM1, and e-selectin-was assessed using a modified ELISA procedure. Cytotoxicity of the alloys was assessed by measuring succinate dehydrogenase (SDH) activity and total protein content of the cells, and nickel release was measured by atomic absorption spectroscopy. Results. None of the alloys suppressed SDH activity or total cellular protein significantly at any surface roughness, indicating little or no cytotoxicity. Ni release was measurable from all alloys, was greatest from the rougher surfaces, and was significantly different for the different alloy types. NiTi alloys exhibited the lowest nickel release. However, none of the alloys activated expression of the CAMs, regardless of surface roughness or nickel release level; Supplemental experiments using nickel ions alone confirmed that ICAM1 was inducible on the endothelial cells by Ni(II) concentrations above 100 μM. Conclusions. In this in vitro system, nickel or other elemental release from several common types of stent alloys was not sufficient to activate expression of CAMs on endothelial surfaces. Although these results indicate a low risk for direct activation of endothelial cells by ions released from stent alloys, other mechanisms, such as modulation of CAM expression by monocytes or smooth muscle cells, must be considered before ion-mediated influence on CAM expression can be dismissed.",
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AU - Wataha, John C.

AU - Lewis, Jill B.

AU - Lockwood, Petra E.

AU - Caughman, Gretchen B

AU - Tseng, Wu Yan

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N2 - Objective. Nickel and cobalt ions activate ICAM1 expression on endothelial cells and keratinocytes. Furthermore, these ions are released in vitro and in vivo from the types of alloys used for vascular stents, but the full biological consequences of this release is not known. In the current study, we determined if release of elements from vascular stent alloys that contained nickel and cobalt was sufficient to activate expression of key cellular adhesion molecules (CAMs) by endothelial cells. Expression of these CAMs is a critical step in the long-term inflammatory response to stent materials and possibly to in-stent restenonsis. Methods. Stainless steel, NiTi, CoCrNi, and NiCr alloys were placed in direct contact with primary human microvascular endothelial cells for 72 hours after preparation at three roughnesses (120, 320, and 1200 grit). Expression of three CAMs-ICAM1, VCAM1, and e-selectin-was assessed using a modified ELISA procedure. Cytotoxicity of the alloys was assessed by measuring succinate dehydrogenase (SDH) activity and total protein content of the cells, and nickel release was measured by atomic absorption spectroscopy. Results. None of the alloys suppressed SDH activity or total cellular protein significantly at any surface roughness, indicating little or no cytotoxicity. Ni release was measurable from all alloys, was greatest from the rougher surfaces, and was significantly different for the different alloy types. NiTi alloys exhibited the lowest nickel release. However, none of the alloys activated expression of the CAMs, regardless of surface roughness or nickel release level; Supplemental experiments using nickel ions alone confirmed that ICAM1 was inducible on the endothelial cells by Ni(II) concentrations above 100 μM. Conclusions. In this in vitro system, nickel or other elemental release from several common types of stent alloys was not sufficient to activate expression of CAMs on endothelial surfaces. Although these results indicate a low risk for direct activation of endothelial cells by ions released from stent alloys, other mechanisms, such as modulation of CAM expression by monocytes or smooth muscle cells, must be considered before ion-mediated influence on CAM expression can be dismissed.

AB - Objective. Nickel and cobalt ions activate ICAM1 expression on endothelial cells and keratinocytes. Furthermore, these ions are released in vitro and in vivo from the types of alloys used for vascular stents, but the full biological consequences of this release is not known. In the current study, we determined if release of elements from vascular stent alloys that contained nickel and cobalt was sufficient to activate expression of key cellular adhesion molecules (CAMs) by endothelial cells. Expression of these CAMs is a critical step in the long-term inflammatory response to stent materials and possibly to in-stent restenonsis. Methods. Stainless steel, NiTi, CoCrNi, and NiCr alloys were placed in direct contact with primary human microvascular endothelial cells for 72 hours after preparation at three roughnesses (120, 320, and 1200 grit). Expression of three CAMs-ICAM1, VCAM1, and e-selectin-was assessed using a modified ELISA procedure. Cytotoxicity of the alloys was assessed by measuring succinate dehydrogenase (SDH) activity and total protein content of the cells, and nickel release was measured by atomic absorption spectroscopy. Results. None of the alloys suppressed SDH activity or total cellular protein significantly at any surface roughness, indicating little or no cytotoxicity. Ni release was measurable from all alloys, was greatest from the rougher surfaces, and was significantly different for the different alloy types. NiTi alloys exhibited the lowest nickel release. However, none of the alloys activated expression of the CAMs, regardless of surface roughness or nickel release level; Supplemental experiments using nickel ions alone confirmed that ICAM1 was inducible on the endothelial cells by Ni(II) concentrations above 100 μM. Conclusions. In this in vitro system, nickel or other elemental release from several common types of stent alloys was not sufficient to activate expression of CAMs on endothelial surfaces. Although these results indicate a low risk for direct activation of endothelial cells by ions released from stent alloys, other mechanisms, such as modulation of CAM expression by monocytes or smooth muscle cells, must be considered before ion-mediated influence on CAM expression can be dismissed.

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