Abstract
Chronic non-healing wounds lead to considerable morbidity and mortality. Pleiotropic effects of high density lipoproteins (HDL) may beneficially affect wound healing. The objectives of this murine study were: (1) to investigate the hypothesis that hypercholesterolemia induces impaired wound healing and (2) to study the effect of topical HDL administration in a model of delayed wound healing. A circular full thickness wound was created on the back of each mouse. A silicone splint was used to counteract wound contraction. Coverage of the wound by granulation tissue and by epithelium was quantified every 2 days. Re-epithelialization from day 0 till day 10 was unexpectedly increased by 21.3% (p < 0.05) in C57BL/6 low density lipoprotein (LDLr) deficient mice with severe hypercholesterolemia (489 ± 14 mg/dL) compared to C57BL/6 mice and this effect was entirely abrogated following cholesterol lowering adenoviral LDLr gene transfer. In contrast, re-epithelialization in hypercholesterolemic (434 ± 16 mg/dL) C57BL/6 apolipoprotein (apo) E−/− mice was 22.6% (p < 0.0001) lower than in C57BL/6 mice. Topical HDL gel administered every 2 days increased re-epithelialization by 25.7% (p < 0.01) in apo E−/− mice. In conclusion, topical HDL application is an innovative therapeutic strategy that corrects impaired wound healing in apo E−/− mice.
Highlights
Decreased high density lipoprotein (HDL) cholesterol levels and elevated non-HDL cholesterol levels are independent risk factors for ischemic cardiovascular diseases [1]
We have previously developed a new method for therapeutic use of HDL, namely topical HDL
Wound coverage by epithelial tissue was very similar in C57BL/6 low density lipoprotein (LDLr)−/−
Summary
Decreased high density lipoprotein (HDL) cholesterol levels and elevated non-HDL cholesterol levels are independent risk factors for ischemic cardiovascular diseases [1] This relationship is very strong for coronary heart disease, but relatively weak for ischemic stroke [1]. HDL increases endothelial progenitor cell (EPC) number and function and this may contribute significantly to its atheroprotective properties [9,10,11]. These pleiotropic effects offer perspectives for new areas for HDL therapy that are outside the field of atherosclerosis and vascular biology. HDL may beneficially affect wound healing by accelerating resolution of inflammation, by enhancing granulation tissue formation involving increased EPC incorporation and increased paracrine effects of EPCs, and by accelerating re-epithelialization
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