Modest effect on plaque progression and vasodilatory function in atherosclerosis-prone mice exposed to nanosized TiO2

Research output: Contribution to journalJournal articleResearchpeer-review

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Modest effect on plaque progression and vasodilatory function in atherosclerosis-prone mice exposed to nanosized TiO2. / Mikkelsen, Lone; Sheykhzade, Majid; Jensen, Keld A; Saber, Anne T; Jacobsen, Nicklas R.; Vogel, Ulla Birgitte; Wallin, Håkan; Loft, Steffen; Møller, Peter.

In: Particle and Fibre Toxicology, Vol. 8, No. 1, 10.11.2011, p. 32.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Mikkelsen, L, Sheykhzade, M, Jensen, KA, Saber, AT, Jacobsen, NR, Vogel, UB, Wallin, H, Loft, S & Møller, P 2011, 'Modest effect on plaque progression and vasodilatory function in atherosclerosis-prone mice exposed to nanosized TiO2', Particle and Fibre Toxicology, vol. 8, no. 1, pp. 32. https://doi.org/10.1186/1743-8977-8-32

APA

Mikkelsen, L., Sheykhzade, M., Jensen, K. A., Saber, A. T., Jacobsen, N. R., Vogel, U. B., ... Møller, P. (2011). Modest effect on plaque progression and vasodilatory function in atherosclerosis-prone mice exposed to nanosized TiO2. Particle and Fibre Toxicology, 8(1), 32. https://doi.org/10.1186/1743-8977-8-32

Vancouver

Mikkelsen L, Sheykhzade M, Jensen KA, Saber AT, Jacobsen NR, Vogel UB et al. Modest effect on plaque progression and vasodilatory function in atherosclerosis-prone mice exposed to nanosized TiO2. Particle and Fibre Toxicology. 2011 Nov 10;8(1):32. https://doi.org/10.1186/1743-8977-8-32

Author

Mikkelsen, Lone ; Sheykhzade, Majid ; Jensen, Keld A ; Saber, Anne T ; Jacobsen, Nicklas R. ; Vogel, Ulla Birgitte ; Wallin, Håkan ; Loft, Steffen ; Møller, Peter. / Modest effect on plaque progression and vasodilatory function in atherosclerosis-prone mice exposed to nanosized TiO2. In: Particle and Fibre Toxicology. 2011 ; Vol. 8, No. 1. pp. 32.

Bibtex

@article{9b3675482a6048cfb1d0f32fb929c048,
title = "Modest effect on plaque progression and vasodilatory function in atherosclerosis-prone mice exposed to nanosized TiO2",
abstract = "ABSTRACT: BACKGROUND: There is growing evidence that exposure to small size particulate matter increases the risk of developing cardiovascular disease. METHODS: We investigated plaque progression and vasodilatory function in apolipoprotein E knockout (ApoE-/-) mice exposed to TiO2. ApoE-/- mice were intratracheally instilled (0.5 mg/kg bodyweight) with rutile fine TiO2 (fTiO2, 288 nm), photocatalytic 92/8 anatase/rutile TiO2 (pTiO2, 12 nm), or rutile nano TiO2 (nTiO2, 21.6 nm) at 26 and 2 hours before measurement of vasodilatory function in aorta segments mounted in myographs. The progression of atherosclerotic plaques in aorta was assessed in mice exposed to nanosized TiO2 (0.5 mg/kg bodyweight) once a week for 4 weeks. We measured mRNA levels of Mcp-1, Mip-2, Vcam-1, Icam-1 and Vegf in lung tissue to assess pulmonary inflammation and vascular function. TiO2-induced alterations in nitric oxide (NO) production were assessed in human umbilical vein endothelial cells (HUVECs). RESULTS: The exposure to nTiO2 was associated with a modest increase in plaque progression in aorta, whereas there were unaltered vasodilatory function and expression levels of Mcp-1, Mip-2, Vcam-1, Icam-1 and Vegf in lung tissue. The ApoE-/- mice exposed to fine and photocatalytic TiO2 had unaltered vasodilatory function and lung tissue inflammatory gene expression. The unaltered NO-dependent vasodilatory function was supported by observations in HUVECs where the NO production was only increased by exposure to nTiO2. CONCLUSION: Repeated exposure to nanosized TiO2 particles was associated with modest plaque progression in ApoE-/- mice. There were no associations between the pulmonary TiO2 exposure and inflammation or vasodilatory dysfunction.",
keywords = "Former Faculty of Pharmaceutical Sciences",
author = "Lone Mikkelsen and Majid Sheykhzade and Jensen, {Keld A} and Saber, {Anne T} and Jacobsen, {Nicklas R.} and Vogel, {Ulla Birgitte} and H{\aa}kan Wallin and Steffen Loft and Peter M{\o}ller",
year = "2011",
month = "11",
day = "10",
doi = "10.1186/1743-8977-8-32",
language = "English",
volume = "8",
pages = "32",
journal = "Particle and Fibre Toxicology",
issn = "1743-8977",
publisher = "BioMed Central",
number = "1",

}

RIS

TY - JOUR

T1 - Modest effect on plaque progression and vasodilatory function in atherosclerosis-prone mice exposed to nanosized TiO2

AU - Mikkelsen, Lone

AU - Sheykhzade, Majid

AU - Jensen, Keld A

AU - Saber, Anne T

AU - Jacobsen, Nicklas R.

AU - Vogel, Ulla Birgitte

AU - Wallin, Håkan

AU - Loft, Steffen

AU - Møller, Peter

PY - 2011/11/10

Y1 - 2011/11/10

N2 - ABSTRACT: BACKGROUND: There is growing evidence that exposure to small size particulate matter increases the risk of developing cardiovascular disease. METHODS: We investigated plaque progression and vasodilatory function in apolipoprotein E knockout (ApoE-/-) mice exposed to TiO2. ApoE-/- mice were intratracheally instilled (0.5 mg/kg bodyweight) with rutile fine TiO2 (fTiO2, 288 nm), photocatalytic 92/8 anatase/rutile TiO2 (pTiO2, 12 nm), or rutile nano TiO2 (nTiO2, 21.6 nm) at 26 and 2 hours before measurement of vasodilatory function in aorta segments mounted in myographs. The progression of atherosclerotic plaques in aorta was assessed in mice exposed to nanosized TiO2 (0.5 mg/kg bodyweight) once a week for 4 weeks. We measured mRNA levels of Mcp-1, Mip-2, Vcam-1, Icam-1 and Vegf in lung tissue to assess pulmonary inflammation and vascular function. TiO2-induced alterations in nitric oxide (NO) production were assessed in human umbilical vein endothelial cells (HUVECs). RESULTS: The exposure to nTiO2 was associated with a modest increase in plaque progression in aorta, whereas there were unaltered vasodilatory function and expression levels of Mcp-1, Mip-2, Vcam-1, Icam-1 and Vegf in lung tissue. The ApoE-/- mice exposed to fine and photocatalytic TiO2 had unaltered vasodilatory function and lung tissue inflammatory gene expression. The unaltered NO-dependent vasodilatory function was supported by observations in HUVECs where the NO production was only increased by exposure to nTiO2. CONCLUSION: Repeated exposure to nanosized TiO2 particles was associated with modest plaque progression in ApoE-/- mice. There were no associations between the pulmonary TiO2 exposure and inflammation or vasodilatory dysfunction.

AB - ABSTRACT: BACKGROUND: There is growing evidence that exposure to small size particulate matter increases the risk of developing cardiovascular disease. METHODS: We investigated plaque progression and vasodilatory function in apolipoprotein E knockout (ApoE-/-) mice exposed to TiO2. ApoE-/- mice were intratracheally instilled (0.5 mg/kg bodyweight) with rutile fine TiO2 (fTiO2, 288 nm), photocatalytic 92/8 anatase/rutile TiO2 (pTiO2, 12 nm), or rutile nano TiO2 (nTiO2, 21.6 nm) at 26 and 2 hours before measurement of vasodilatory function in aorta segments mounted in myographs. The progression of atherosclerotic plaques in aorta was assessed in mice exposed to nanosized TiO2 (0.5 mg/kg bodyweight) once a week for 4 weeks. We measured mRNA levels of Mcp-1, Mip-2, Vcam-1, Icam-1 and Vegf in lung tissue to assess pulmonary inflammation and vascular function. TiO2-induced alterations in nitric oxide (NO) production were assessed in human umbilical vein endothelial cells (HUVECs). RESULTS: The exposure to nTiO2 was associated with a modest increase in plaque progression in aorta, whereas there were unaltered vasodilatory function and expression levels of Mcp-1, Mip-2, Vcam-1, Icam-1 and Vegf in lung tissue. The ApoE-/- mice exposed to fine and photocatalytic TiO2 had unaltered vasodilatory function and lung tissue inflammatory gene expression. The unaltered NO-dependent vasodilatory function was supported by observations in HUVECs where the NO production was only increased by exposure to nTiO2. CONCLUSION: Repeated exposure to nanosized TiO2 particles was associated with modest plaque progression in ApoE-/- mice. There were no associations between the pulmonary TiO2 exposure and inflammation or vasodilatory dysfunction.

KW - Former Faculty of Pharmaceutical Sciences

U2 - 10.1186/1743-8977-8-32

DO - 10.1186/1743-8977-8-32

M3 - Journal article

C2 - 22074227

VL - 8

SP - 32

JO - Particle and Fibre Toxicology

JF - Particle and Fibre Toxicology

SN - 1743-8977

IS - 1

ER -

ID: 35317522