Interactions between stainless steel, shear stress, and monocytes

Regina L W Messer, John Mickalonis, Jill B. Lewis, Yo Omata, Cortney M. Davis, Yolanda Brown, John C. Wataha

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Angioplasty with stent placement is commonly used to treat coronary atherosclerosis. However, 20-40% of stainless steel stents restenose within 6 months via a prolonged inflammatory response mediated by monocytic infiltration and cytokine secretion. In the current study, we tested a hypothesis that blood flow and monocytes interact to alter stent corrosion. We assessed the effects of THP1 monocytes on the corrosion rate of 316L stainless steel (316LSS) under shear stress (0.5-50 dyn/cm2). In addition, THP1 cytokine secretion was determined using cytokine arrays and ELISA analyses. Data were compared using ANOVA and Tukey post hoc analysis (a = 0.05). Monocytes significantly lowered 316LSS corrosion rates without limiting current density. However, shear stress alone did not alter the corrosion rate of 316LSS. THP1 cells adhered to the 316LSS surface at all flow rates. Exposure to the 316LSS/corrosion test under high fluid flow rates increased (>twofold) the secretion of 7 of the 42 cytokines tested (angeogenin, GRO, 1309, interleukin 8, interleukin 6, interleukin 1β, and macrophage chemoattractant protein-1). Each of these cytokines play a role in wound healing, macrophage differentiation, and cell proliferation, all hallmarks of in-stent restenosis. Furthermore, only IL8 levels were significantly higher than any of the system controls during the 316LSS/corrosion test conditions. The IL8 levels from the 316LSS/corrosion tests were not significantly different from the +LPS control. Together, these data suggest that monocytic cells maybe activated by exposure to 316LSS stents and could contribute to in-stent restenosis and altered corrosion of the stent.

Original languageEnglish (US)
Pages (from-to)229-235
Number of pages7
JournalJournal of Biomedical Materials Research - Part A
Volume87
Issue number1
DOIs
StatePublished - Oct 1 2008

Fingerprint

Stainless Steel
Corrosion
Stents
Shear stress
Monocytes
Stainless steel
Steel corrosion
Cytokines
Corrosion rate
Interleukin-8
Macrophages
Flow rate
Chemotactic Factors
Cell proliferation
Analysis of variance (ANOVA)
Interleukin-1
Angioplasty
Infiltration
Wound Healing
Flow of fluids

Keywords

  • Cardiovascular
  • Corrosion
  • In-stent restenosis
  • Monocyte
  • Shear
  • Stainless steel
  • Stent
  • THP
  • THP1

ASJC Scopus subject areas

  • Ceramics and Composites
  • Biomaterials
  • Biomedical Engineering
  • Metals and Alloys

Cite this

Messer, R. L. W., Mickalonis, J., Lewis, J. B., Omata, Y., Davis, C. M., Brown, Y., & Wataha, J. C. (2008). Interactions between stainless steel, shear stress, and monocytes. Journal of Biomedical Materials Research - Part A, 87(1), 229-235. https://doi.org/10.1002/jbm.a.31730

Interactions between stainless steel, shear stress, and monocytes. / Messer, Regina L W; Mickalonis, John; Lewis, Jill B.; Omata, Yo; Davis, Cortney M.; Brown, Yolanda; Wataha, John C.

In: Journal of Biomedical Materials Research - Part A, Vol. 87, No. 1, 01.10.2008, p. 229-235.

Research output: Contribution to journalArticle

Messer, RLW, Mickalonis, J, Lewis, JB, Omata, Y, Davis, CM, Brown, Y & Wataha, JC 2008, 'Interactions between stainless steel, shear stress, and monocytes', Journal of Biomedical Materials Research - Part A, vol. 87, no. 1, pp. 229-235. https://doi.org/10.1002/jbm.a.31730
Messer, Regina L W ; Mickalonis, John ; Lewis, Jill B. ; Omata, Yo ; Davis, Cortney M. ; Brown, Yolanda ; Wataha, John C. / Interactions between stainless steel, shear stress, and monocytes. In: Journal of Biomedical Materials Research - Part A. 2008 ; Vol. 87, No. 1. pp. 229-235.
@article{d769f09991cb4490850f1951051dd5d7,
title = "Interactions between stainless steel, shear stress, and monocytes",
abstract = "Angioplasty with stent placement is commonly used to treat coronary atherosclerosis. However, 20-40{\%} of stainless steel stents restenose within 6 months via a prolonged inflammatory response mediated by monocytic infiltration and cytokine secretion. In the current study, we tested a hypothesis that blood flow and monocytes interact to alter stent corrosion. We assessed the effects of THP1 monocytes on the corrosion rate of 316L stainless steel (316LSS) under shear stress (0.5-50 dyn/cm2). In addition, THP1 cytokine secretion was determined using cytokine arrays and ELISA analyses. Data were compared using ANOVA and Tukey post hoc analysis (a = 0.05). Monocytes significantly lowered 316LSS corrosion rates without limiting current density. However, shear stress alone did not alter the corrosion rate of 316LSS. THP1 cells adhered to the 316LSS surface at all flow rates. Exposure to the 316LSS/corrosion test under high fluid flow rates increased (>twofold) the secretion of 7 of the 42 cytokines tested (angeogenin, GRO, 1309, interleukin 8, interleukin 6, interleukin 1β, and macrophage chemoattractant protein-1). Each of these cytokines play a role in wound healing, macrophage differentiation, and cell proliferation, all hallmarks of in-stent restenosis. Furthermore, only IL8 levels were significantly higher than any of the system controls during the 316LSS/corrosion test conditions. The IL8 levels from the 316LSS/corrosion tests were not significantly different from the +LPS control. Together, these data suggest that monocytic cells maybe activated by exposure to 316LSS stents and could contribute to in-stent restenosis and altered corrosion of the stent.",
keywords = "Cardiovascular, Corrosion, In-stent restenosis, Monocyte, Shear, Stainless steel, Stent, THP, THP1",
author = "Messer, {Regina L W} and John Mickalonis and Lewis, {Jill B.} and Yo Omata and Davis, {Cortney M.} and Yolanda Brown and Wataha, {John C.}",
year = "2008",
month = "10",
day = "1",
doi = "10.1002/jbm.a.31730",
language = "English (US)",
volume = "87",
pages = "229--235",
journal = "Journal of Biomedical Materials Research - Part A",
issn = "0021-9304",
publisher = "Heterocorporation",
number = "1",

}

TY - JOUR

T1 - Interactions between stainless steel, shear stress, and monocytes

AU - Messer, Regina L W

AU - Mickalonis, John

AU - Lewis, Jill B.

AU - Omata, Yo

AU - Davis, Cortney M.

AU - Brown, Yolanda

AU - Wataha, John C.

PY - 2008/10/1

Y1 - 2008/10/1

N2 - Angioplasty with stent placement is commonly used to treat coronary atherosclerosis. However, 20-40% of stainless steel stents restenose within 6 months via a prolonged inflammatory response mediated by monocytic infiltration and cytokine secretion. In the current study, we tested a hypothesis that blood flow and monocytes interact to alter stent corrosion. We assessed the effects of THP1 monocytes on the corrosion rate of 316L stainless steel (316LSS) under shear stress (0.5-50 dyn/cm2). In addition, THP1 cytokine secretion was determined using cytokine arrays and ELISA analyses. Data were compared using ANOVA and Tukey post hoc analysis (a = 0.05). Monocytes significantly lowered 316LSS corrosion rates without limiting current density. However, shear stress alone did not alter the corrosion rate of 316LSS. THP1 cells adhered to the 316LSS surface at all flow rates. Exposure to the 316LSS/corrosion test under high fluid flow rates increased (>twofold) the secretion of 7 of the 42 cytokines tested (angeogenin, GRO, 1309, interleukin 8, interleukin 6, interleukin 1β, and macrophage chemoattractant protein-1). Each of these cytokines play a role in wound healing, macrophage differentiation, and cell proliferation, all hallmarks of in-stent restenosis. Furthermore, only IL8 levels were significantly higher than any of the system controls during the 316LSS/corrosion test conditions. The IL8 levels from the 316LSS/corrosion tests were not significantly different from the +LPS control. Together, these data suggest that monocytic cells maybe activated by exposure to 316LSS stents and could contribute to in-stent restenosis and altered corrosion of the stent.

AB - Angioplasty with stent placement is commonly used to treat coronary atherosclerosis. However, 20-40% of stainless steel stents restenose within 6 months via a prolonged inflammatory response mediated by monocytic infiltration and cytokine secretion. In the current study, we tested a hypothesis that blood flow and monocytes interact to alter stent corrosion. We assessed the effects of THP1 monocytes on the corrosion rate of 316L stainless steel (316LSS) under shear stress (0.5-50 dyn/cm2). In addition, THP1 cytokine secretion was determined using cytokine arrays and ELISA analyses. Data were compared using ANOVA and Tukey post hoc analysis (a = 0.05). Monocytes significantly lowered 316LSS corrosion rates without limiting current density. However, shear stress alone did not alter the corrosion rate of 316LSS. THP1 cells adhered to the 316LSS surface at all flow rates. Exposure to the 316LSS/corrosion test under high fluid flow rates increased (>twofold) the secretion of 7 of the 42 cytokines tested (angeogenin, GRO, 1309, interleukin 8, interleukin 6, interleukin 1β, and macrophage chemoattractant protein-1). Each of these cytokines play a role in wound healing, macrophage differentiation, and cell proliferation, all hallmarks of in-stent restenosis. Furthermore, only IL8 levels were significantly higher than any of the system controls during the 316LSS/corrosion test conditions. The IL8 levels from the 316LSS/corrosion tests were not significantly different from the +LPS control. Together, these data suggest that monocytic cells maybe activated by exposure to 316LSS stents and could contribute to in-stent restenosis and altered corrosion of the stent.

KW - Cardiovascular

KW - Corrosion

KW - In-stent restenosis

KW - Monocyte

KW - Shear

KW - Stainless steel

KW - Stent

KW - THP

KW - THP1

UR - http://www.scopus.com/inward/record.url?scp=51849112724&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=51849112724&partnerID=8YFLogxK

U2 - 10.1002/jbm.a.31730

DO - 10.1002/jbm.a.31730

M3 - Article

VL - 87

SP - 229

EP - 235

JO - Journal of Biomedical Materials Research - Part A

JF - Journal of Biomedical Materials Research - Part A

SN - 0021-9304

IS - 1

ER -