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

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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.

I: Particle and Fibre Toxicology, Bind 8, Nr. 1, 10.11.2011, s. 32.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

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, bind 8, nr. 1, s. 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., 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, 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 o.a. 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. I: Particle and Fibre Toxicology. 2011 ; Bind 8, Nr. 1. s. 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 = nov,
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