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• W2024296744 abstract "Introduction: Progressive peripheral arterial disease is associated with tremendous morbidity and mortality. Non-reconstructable disease leads to limb loss and permanent disability. Multiple clinical trials have examined the use of angiogenic factors to improve angiogenesis and limb salvage. However, none has reached clinical application. Heme oxygenase-1 (HO-1) is induced by stressful stimuli and has been reported to stimulate angiogenesis in vitro and in retinal ischemia models. Carbon monoxide (CO) is a by-product of HO-1 metabolism and mediates HO-1's actions. Therefore, we hypothesize that CO may have pro-angiogenic properties and enhance angiogenesis. Methods: Human umbilical vein endothelial cells (HUVEC) were cultured in growth factor reduced (GFR) Matrigel under serum depleted conditions (1% FBS in DMEM) in a CO chamber delivering CO at 250 PPM or in a traditional incubator. EC tube formation was assessed at 6 hrs. Cell migration was assessed using the Boyden chamber. C3H mice underwent unilateral femoral artery ligation/resection to create hindlimb ischemia. Experimental mice received inhaled CO (250 PPM) for 1 hr prior to femoral ligation and daily until sacrifice. Laser doppler perfusion imaging (LDPI) was used to assess perfusion at different time points. Data was presented as ischemic/contralateral limb perfusion. Mice were sacrificed at 2 or 4 wks and the anterior tibialis muscle was examined histologically for viability and regeneration. Results: HUVEC exposed to CO showed a 33% increase in migration (p<0.001 vs control, experiment repeated x3). CO also increased EC tube formation by 6 hrs. In the hindlimb ischemia model, mice treated with inhaled CO experienced less skeletal muscle injury and fat replacement compared to air treated mice, suggesting reduced ischemic muscle injury. At 2 wks, LDPI revealed significantly lower limb perfusion in CO treated mice versus the control mice (Figure, p = 0.034, n=6-7/group). However, limb perfusion for both groups was near identical by 4 wks. Conclusions: CO enhances EC migration and tube formation in vitro. CO treatment delayed restoration of perfusion in the ischemic hindlimb but was protective against ischemic skeletal muscle injury. These findings suggest that CO does have pro-angiogenic properties in ECs. While CO did not increase tissue perfusion, it did protect against ischemic muscle injury which may reduce the angiogenic drive. Further studies are necessary to separate the cytoprotective functions of CO from its potential functions in angiogenesis." @default.
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• W2024296744 date "2011-02-01" @default.
• W2024296744 modified "2023-09-27" @default.
• W2024296744 title "Inhaled Carbon Monoxide Protects Skeletal Muscle from Ischemic Injury in a Murine Model of Hindlimb Ischemia Without Improving Angiogenesis" @default.
• W2024296744 doi "https://doi.org/10.1016/j.jss.2010.11.488" @default.
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