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Abstract
Endothelial progenitor cells (EPC) participate in vessel recovery and maintenance of normal endothelial function. Therefore, pitavastatin-nanoparticles (NPs)-engineered EPC may be effective in repairing injured vasculature. Pitavastatin-loaded poly(lactic-co-glycolic) acid (PLGA) NPs were obtained via ultrasonic emulsion solvent evaporation with PLGA as the carrier encapsulating pitavastatin. The effects and mechanism of pitavastatin-NPs on EPC proliferation in vitro were evaluated. Then, EPC that internalized pitavastatin-NPs were transplanted into rats after carotid artery injury. EPC homing, re-endothelialization, and neointima were evaluated by fluorescence labeling, evans Blue and hematoxylin/eosin (H&E) staining. Pitavastatin-NPs significantly improved EPC proliferation compared with control and pitavastatin group. Those effects were blocked by pretreatment with the pharmacological phosphoinositide 3-kinase (PI3K) blockers LY294002. After carotid artery injury, more transplanted EPC were detected in target zone in Pitavastatin-NPs group than pitavastatin and control group. Re-endothelialization was promoted and intimal hyperplasia was inhibited as well. Thus, pitavastatin-NPs promote EPC proliferation via PI3K signaling and accelerate recovery of injured carotid artery.
Highlights
Vascular endothelial injury is the main pathophysiological basis for atherosclerotic diseases and restenosis after coronary intervention[1]
The concentration of pitavastatin in pitavastatin-NPs was determined by High-performance liquid chromatography (HPLC)
This study for the first time reported that pitavastatin promoted Endothelial progenitor cells (EPC) proliferation via phosphoinositide 3-kinase (PI3K) signaling and pitavastatin nanoparticle-engineered EPC accelerated vessel recovery after carotid artery injury in rats
Summary
Vascular endothelial injury is the main pathophysiological basis for atherosclerotic diseases and restenosis after coronary intervention[1]. Statins are the most widely used agent for treatment of ischemic cardiovascular disease. They have cardioprotective effects independent of their lipid-lowering function that includes improving the biological function of EPC5. These pleiotropic effects require long-term administration of high statin dosages[6,7], which is limited by relatively low oral bioavailability and lead to an increased risk of adverse reactions[8,9]. Pitavastatin is a new-generation statin that has greater efficacy in terms of lipid regulation, improvement of endothelial function, and plaque regression. We investigate the effect and mechanism of pitavastatin-NPs on EPC proliferation and vessel repair
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