Overexpression of catalase in myeloid cells causes impaired postischemic neovascularization

Roberto Hodara, Daiana Weiss, Giji Joseph, Juan C. Velasquez-Castano, Natalia Landázuri, Ji Woong Han, Youngsup Yoon, W. Robert Taylor

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

OBJECTIVE-: Myeloid lineage cells (MLCs) such as macrophages are known to play a key role in postischemic neovascularization. However, the role of MLC-derived reactive oxygen species in this process and their specific chemical identity remain unknown. METHODS AND RESULTS-: Transgenic mice with MLC-specific overexpression of catalase (TgCat-MLC mice) were created on a C57BL/6 background. Macrophage catalase activity was increased 3.4-fold compared with wild-type mice. After femoral artery ligation, laser Doppler perfusion imaging revealed impaired perfusion recovery in TgCat-MLC mice. This was associated with fewer collateral vessels, as assessed by microcomputed tomography angiography, and decreased capillary density. Impaired functional recovery of the ischemic limb was also evidenced by a 50% reduction in spontaneous running activity. The deficient neovascularization was associated with a blunted inflammatory response, characterized by decreased macrophage infiltration of ischemic tissues, and lower mRNA levels of inflammatory markers, such as tumor necrosis factor-α, osteopontin, and matrix mettaloproteinase-9. In vitro macrophage migration was impaired in Tg mice, suggesting a role for H2O2 in regulating the ability of macrophages to infiltrate ischemic tissues. CONCLUSION-: MLC-derived H 2O2 plays a key role in promoting neovascularization in response to ischemia and is a necessary factor for the development of ischemia-induced inflammation.

Original languageEnglish
Pages (from-to)2203-2209
Number of pages7
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Volume31
Issue number10
DOIs
Publication statusPublished - 2011 Oct 1

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Myeloid Cells
Catalase
Macrophages
Ischemia
X-Ray Microtomography
Osteopontin
Perfusion Imaging
Femoral Artery
Running
Transgenic Mice
Ligation
Reactive Oxygen Species
Angiography
Lasers
Extremities
Tumor Necrosis Factor-alpha
Perfusion
Inflammation
Messenger RNA

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Hodara, R., Weiss, D., Joseph, G., Velasquez-Castano, J. C., Landázuri, N., Han, J. W., ... Taylor, W. R. (2011). Overexpression of catalase in myeloid cells causes impaired postischemic neovascularization. Arteriosclerosis, Thrombosis, and Vascular Biology, 31(10), 2203-2209. https://doi.org/10.1161/ATVBAHA.111.233247
Hodara, Roberto ; Weiss, Daiana ; Joseph, Giji ; Velasquez-Castano, Juan C. ; Landázuri, Natalia ; Han, Ji Woong ; Yoon, Youngsup ; Taylor, W. Robert. / Overexpression of catalase in myeloid cells causes impaired postischemic neovascularization. In: Arteriosclerosis, Thrombosis, and Vascular Biology. 2011 ; Vol. 31, No. 10. pp. 2203-2209.
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abstract = "OBJECTIVE-: Myeloid lineage cells (MLCs) such as macrophages are known to play a key role in postischemic neovascularization. However, the role of MLC-derived reactive oxygen species in this process and their specific chemical identity remain unknown. METHODS AND RESULTS-: Transgenic mice with MLC-specific overexpression of catalase (TgCat-MLC mice) were created on a C57BL/6 background. Macrophage catalase activity was increased 3.4-fold compared with wild-type mice. After femoral artery ligation, laser Doppler perfusion imaging revealed impaired perfusion recovery in TgCat-MLC mice. This was associated with fewer collateral vessels, as assessed by microcomputed tomography angiography, and decreased capillary density. Impaired functional recovery of the ischemic limb was also evidenced by a 50{\%} reduction in spontaneous running activity. The deficient neovascularization was associated with a blunted inflammatory response, characterized by decreased macrophage infiltration of ischemic tissues, and lower mRNA levels of inflammatory markers, such as tumor necrosis factor-α, osteopontin, and matrix mettaloproteinase-9. In vitro macrophage migration was impaired in Tg mice, suggesting a role for H2O2 in regulating the ability of macrophages to infiltrate ischemic tissues. CONCLUSION-: MLC-derived H 2O2 plays a key role in promoting neovascularization in response to ischemia and is a necessary factor for the development of ischemia-induced inflammation.",
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Hodara, R, Weiss, D, Joseph, G, Velasquez-Castano, JC, Landázuri, N, Han, JW, Yoon, Y & Taylor, WR 2011, 'Overexpression of catalase in myeloid cells causes impaired postischemic neovascularization', Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 31, no. 10, pp. 2203-2209. https://doi.org/10.1161/ATVBAHA.111.233247

Overexpression of catalase in myeloid cells causes impaired postischemic neovascularization. / Hodara, Roberto; Weiss, Daiana; Joseph, Giji; Velasquez-Castano, Juan C.; Landázuri, Natalia; Han, Ji Woong; Yoon, Youngsup; Taylor, W. Robert.

In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 31, No. 10, 01.10.2011, p. 2203-2209.

Research output: Contribution to journalArticle

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T1 - Overexpression of catalase in myeloid cells causes impaired postischemic neovascularization

AU - Hodara, Roberto

AU - Weiss, Daiana

AU - Joseph, Giji

AU - Velasquez-Castano, Juan C.

AU - Landázuri, Natalia

AU - Han, Ji Woong

AU - Yoon, Youngsup

AU - Taylor, W. Robert

PY - 2011/10/1

Y1 - 2011/10/1

N2 - OBJECTIVE-: Myeloid lineage cells (MLCs) such as macrophages are known to play a key role in postischemic neovascularization. However, the role of MLC-derived reactive oxygen species in this process and their specific chemical identity remain unknown. METHODS AND RESULTS-: Transgenic mice with MLC-specific overexpression of catalase (TgCat-MLC mice) were created on a C57BL/6 background. Macrophage catalase activity was increased 3.4-fold compared with wild-type mice. After femoral artery ligation, laser Doppler perfusion imaging revealed impaired perfusion recovery in TgCat-MLC mice. This was associated with fewer collateral vessels, as assessed by microcomputed tomography angiography, and decreased capillary density. Impaired functional recovery of the ischemic limb was also evidenced by a 50% reduction in spontaneous running activity. The deficient neovascularization was associated with a blunted inflammatory response, characterized by decreased macrophage infiltration of ischemic tissues, and lower mRNA levels of inflammatory markers, such as tumor necrosis factor-α, osteopontin, and matrix mettaloproteinase-9. In vitro macrophage migration was impaired in Tg mice, suggesting a role for H2O2 in regulating the ability of macrophages to infiltrate ischemic tissues. CONCLUSION-: MLC-derived H 2O2 plays a key role in promoting neovascularization in response to ischemia and is a necessary factor for the development of ischemia-induced inflammation.

AB - OBJECTIVE-: Myeloid lineage cells (MLCs) such as macrophages are known to play a key role in postischemic neovascularization. However, the role of MLC-derived reactive oxygen species in this process and their specific chemical identity remain unknown. METHODS AND RESULTS-: Transgenic mice with MLC-specific overexpression of catalase (TgCat-MLC mice) were created on a C57BL/6 background. Macrophage catalase activity was increased 3.4-fold compared with wild-type mice. After femoral artery ligation, laser Doppler perfusion imaging revealed impaired perfusion recovery in TgCat-MLC mice. This was associated with fewer collateral vessels, as assessed by microcomputed tomography angiography, and decreased capillary density. Impaired functional recovery of the ischemic limb was also evidenced by a 50% reduction in spontaneous running activity. The deficient neovascularization was associated with a blunted inflammatory response, characterized by decreased macrophage infiltration of ischemic tissues, and lower mRNA levels of inflammatory markers, such as tumor necrosis factor-α, osteopontin, and matrix mettaloproteinase-9. In vitro macrophage migration was impaired in Tg mice, suggesting a role for H2O2 in regulating the ability of macrophages to infiltrate ischemic tissues. CONCLUSION-: MLC-derived H 2O2 plays a key role in promoting neovascularization in response to ischemia and is a necessary factor for the development of ischemia-induced inflammation.

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