Macrophage depletion by clodronate liposomes suppresses neointimal formation after carotid artery injury in apolipoprotein E-deficient mice

Soon Jun Hong, Hoon Ahn Tae, Wan Joo Shim, Seong-Mi Park, Il Choi Jong, Suk Park Jae, Sang Yeob Lim, Do-Sun Lim, Chang Gyu Park, Hong Seog Seo

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1 Citation (Scopus)

Abstract

Background and Objectives: Clodronate liposomes deplete phagocytic cells, thereby suppressing inflammation after vascular injury. We compared the effect of clodronate liposomes on macrophage depletion and neointimal formation in apolipoprotein E-deficient mice [ApoE (-) mice]. Materials and Methods: ApoE (-) mice were randomly assigned to the clodronate liposomes group (Clodronate Group, n = 7) and the vehicle liposomes group (Control Group, n=7). Clodronate (0.1 mL/10 g) was injected via the tail vein starting 2 days (d-2) before left common carotid artery injury. Results: The percentage of blood monocytes was subsequently decreased after clodronate injection (14.0 ± 7.4% at baseline, 6.8 ± 4.9% at 24 hours and 0.7 ± 0.3% at 1 week after the clodronate liposome injection). The percentage of macrophages in the plaque area was significantly lower in the clodronate group at week 2 (32.0 ± 6.5 vs. 68.7 ± 7.6%, respectively, p < 0.05) and at week 4 (37.3 ± 8.5 vs. 62.6 ± 9.4%, respectively, p < 0.05). The interleukin (IL)-6 and tumor necrosis factor (TNF)-α concentrations were significantly decreased in the clodronate group at week 4 (12.3 ± 2.5 vs. 22.9 ± 3.5 pg/mL, respectively, p < 0.05 for IL-6 and 16.6 ± 2.2 vs. 43.6 ± 6.1 pg/mL, respectively, p < 0.05 for TNF-α). The plaque volume was significantly greater in the control group at week 2 (0.345 ± 0.063 vs. 0.153 ± 0.053 mm 2, respectively, p < 0.05) and at week 4 (0.320 ± 0.027 vs. 0.167 ± 0.070 mm 2, respectively, p < 0.05). Conclusion: Intravenous administration of clodronate liposomes depleted monocytes and macrophages, and so this reduced the inflammatory markers and neointimal formation in ApoE (-) mice.

Original languageEnglish
Pages (from-to)244-249
Number of pages6
JournalKorean Circulation Journal
Volume38
Issue number5
DOIs
Publication statusPublished - 2008 May 1

Fingerprint

Carotid Artery Injuries
Clodronic Acid
Apolipoproteins E
Liposomes
Macrophages
Monocytes
Interleukin-6
Tumor Necrosis Factor-alpha
Control Groups
Injections
Vascular System Injuries
Common Carotid Artery
Phagocytes
Intravenous Administration
Tail
Veins

Keywords

  • Clodronate
  • Inflammation
  • Macrophages

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Internal Medicine

Cite this

@article{47a8658823c444c1b75e27a908f804db,
title = "Macrophage depletion by clodronate liposomes suppresses neointimal formation after carotid artery injury in apolipoprotein E-deficient mice",
abstract = "Background and Objectives: Clodronate liposomes deplete phagocytic cells, thereby suppressing inflammation after vascular injury. We compared the effect of clodronate liposomes on macrophage depletion and neointimal formation in apolipoprotein E-deficient mice [ApoE (-) mice]. Materials and Methods: ApoE (-) mice were randomly assigned to the clodronate liposomes group (Clodronate Group, n = 7) and the vehicle liposomes group (Control Group, n=7). Clodronate (0.1 mL/10 g) was injected via the tail vein starting 2 days (d-2) before left common carotid artery injury. Results: The percentage of blood monocytes was subsequently decreased after clodronate injection (14.0 ± 7.4{\%} at baseline, 6.8 ± 4.9{\%} at 24 hours and 0.7 ± 0.3{\%} at 1 week after the clodronate liposome injection). The percentage of macrophages in the plaque area was significantly lower in the clodronate group at week 2 (32.0 ± 6.5 vs. 68.7 ± 7.6{\%}, respectively, p < 0.05) and at week 4 (37.3 ± 8.5 vs. 62.6 ± 9.4{\%}, respectively, p < 0.05). The interleukin (IL)-6 and tumor necrosis factor (TNF)-α concentrations were significantly decreased in the clodronate group at week 4 (12.3 ± 2.5 vs. 22.9 ± 3.5 pg/mL, respectively, p < 0.05 for IL-6 and 16.6 ± 2.2 vs. 43.6 ± 6.1 pg/mL, respectively, p < 0.05 for TNF-α). The plaque volume was significantly greater in the control group at week 2 (0.345 ± 0.063 vs. 0.153 ± 0.053 mm 2, respectively, p < 0.05) and at week 4 (0.320 ± 0.027 vs. 0.167 ± 0.070 mm 2, respectively, p < 0.05). Conclusion: Intravenous administration of clodronate liposomes depleted monocytes and macrophages, and so this reduced the inflammatory markers and neointimal formation in ApoE (-) mice.",
keywords = "Clodronate, Inflammation, Macrophages",
author = "Hong, {Soon Jun} and Tae, {Hoon Ahn} and Shim, {Wan Joo} and Seong-Mi Park and Jong, {Il Choi} and Jae, {Suk Park} and Lim, {Sang Yeob} and Do-Sun Lim and Park, {Chang Gyu} and Seo, {Hong Seog}",
year = "2008",
month = "5",
day = "1",
doi = "10.4070/kcj.2008.38.5.244",
language = "English",
volume = "38",
pages = "244--249",
journal = "Korean Circulation Journal",
issn = "1738-5520",
publisher = "Korean Society of Circulation",
number = "5",

}

TY - JOUR

T1 - Macrophage depletion by clodronate liposomes suppresses neointimal formation after carotid artery injury in apolipoprotein E-deficient mice

AU - Hong, Soon Jun

AU - Tae, Hoon Ahn

AU - Shim, Wan Joo

AU - Park, Seong-Mi

AU - Jong, Il Choi

AU - Jae, Suk Park

AU - Lim, Sang Yeob

AU - Lim, Do-Sun

AU - Park, Chang Gyu

AU - Seo, Hong Seog

PY - 2008/5/1

Y1 - 2008/5/1

N2 - Background and Objectives: Clodronate liposomes deplete phagocytic cells, thereby suppressing inflammation after vascular injury. We compared the effect of clodronate liposomes on macrophage depletion and neointimal formation in apolipoprotein E-deficient mice [ApoE (-) mice]. Materials and Methods: ApoE (-) mice were randomly assigned to the clodronate liposomes group (Clodronate Group, n = 7) and the vehicle liposomes group (Control Group, n=7). Clodronate (0.1 mL/10 g) was injected via the tail vein starting 2 days (d-2) before left common carotid artery injury. Results: The percentage of blood monocytes was subsequently decreased after clodronate injection (14.0 ± 7.4% at baseline, 6.8 ± 4.9% at 24 hours and 0.7 ± 0.3% at 1 week after the clodronate liposome injection). The percentage of macrophages in the plaque area was significantly lower in the clodronate group at week 2 (32.0 ± 6.5 vs. 68.7 ± 7.6%, respectively, p < 0.05) and at week 4 (37.3 ± 8.5 vs. 62.6 ± 9.4%, respectively, p < 0.05). The interleukin (IL)-6 and tumor necrosis factor (TNF)-α concentrations were significantly decreased in the clodronate group at week 4 (12.3 ± 2.5 vs. 22.9 ± 3.5 pg/mL, respectively, p < 0.05 for IL-6 and 16.6 ± 2.2 vs. 43.6 ± 6.1 pg/mL, respectively, p < 0.05 for TNF-α). The plaque volume was significantly greater in the control group at week 2 (0.345 ± 0.063 vs. 0.153 ± 0.053 mm 2, respectively, p < 0.05) and at week 4 (0.320 ± 0.027 vs. 0.167 ± 0.070 mm 2, respectively, p < 0.05). Conclusion: Intravenous administration of clodronate liposomes depleted monocytes and macrophages, and so this reduced the inflammatory markers and neointimal formation in ApoE (-) mice.

AB - Background and Objectives: Clodronate liposomes deplete phagocytic cells, thereby suppressing inflammation after vascular injury. We compared the effect of clodronate liposomes on macrophage depletion and neointimal formation in apolipoprotein E-deficient mice [ApoE (-) mice]. Materials and Methods: ApoE (-) mice were randomly assigned to the clodronate liposomes group (Clodronate Group, n = 7) and the vehicle liposomes group (Control Group, n=7). Clodronate (0.1 mL/10 g) was injected via the tail vein starting 2 days (d-2) before left common carotid artery injury. Results: The percentage of blood monocytes was subsequently decreased after clodronate injection (14.0 ± 7.4% at baseline, 6.8 ± 4.9% at 24 hours and 0.7 ± 0.3% at 1 week after the clodronate liposome injection). The percentage of macrophages in the plaque area was significantly lower in the clodronate group at week 2 (32.0 ± 6.5 vs. 68.7 ± 7.6%, respectively, p < 0.05) and at week 4 (37.3 ± 8.5 vs. 62.6 ± 9.4%, respectively, p < 0.05). The interleukin (IL)-6 and tumor necrosis factor (TNF)-α concentrations were significantly decreased in the clodronate group at week 4 (12.3 ± 2.5 vs. 22.9 ± 3.5 pg/mL, respectively, p < 0.05 for IL-6 and 16.6 ± 2.2 vs. 43.6 ± 6.1 pg/mL, respectively, p < 0.05 for TNF-α). The plaque volume was significantly greater in the control group at week 2 (0.345 ± 0.063 vs. 0.153 ± 0.053 mm 2, respectively, p < 0.05) and at week 4 (0.320 ± 0.027 vs. 0.167 ± 0.070 mm 2, respectively, p < 0.05). Conclusion: Intravenous administration of clodronate liposomes depleted monocytes and macrophages, and so this reduced the inflammatory markers and neointimal formation in ApoE (-) mice.

KW - Clodronate

KW - Inflammation

KW - Macrophages

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U2 - 10.4070/kcj.2008.38.5.244

DO - 10.4070/kcj.2008.38.5.244

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VL - 38

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JF - Korean Circulation Journal

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