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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  ;  Young-sup Yoon  ;  W Robert Taylor 
 Arteriosclerosis Thromobosis and Vascular Biology, Vol.31(10) : 2203-2209, 2011 
Journal Title
 Arteriosclerosis Thromobosis and Vascular Biology 
Issue Date
Animals ; Capillaries/diagnostic imaging ; Capillaries/enzymology* ; Capillaries/physiopathology ; Catalase/biosynthesis* ; Catalase/genetics ; Cell Movement ; Cells, Cultured ; Collateral Circulation ; Disease Models, Animal ; Endothelial Cells/metabolism ; Femoral Artery/surgery ; Genotype ; Hindlimb ; Humans ; Hydrogen Peroxide/metabolism* ; Inflammation Mediators/metabolism ; Ischemia/enzymology* ; Ischemia/genetics ; Ischemia/physiopathology ; Laser-Doppler Flowmetry ; Ligation ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Motor Activity ; Muscle, Skeletal/blood supply* ; Myeloid Cells/enzymology* ; Neovascularization, Physiologic*/genetics ; Phenotype ; RNA, Messenger/metabolism ; Regional Blood Flow ; Stem Cells/metabolism ; Time Factors ; Ultrasonography ; Up-Regulation ; X-Ray Microtomography
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 (Tg(Cat-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 Tg(Cat-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(Cat-MLC) mice, suggesting a role for H(2)O(2) in regulating the ability of macrophages to infiltrate ischemic tissues. CONCLUSIONS : MLC-derived H(2)O(2) 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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Yonsei Authors
Yoon, Young Sup(윤영섭)
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