Nitric oxide-releasing nanoparticles accelerate wound healing by promoting fibroblast migration and collagen deposition.
Wound healing is a complex process that involves coordinated interactions between diverse immunological and biological systems. Long-term wounds remain a challenging clinical problem, affecting approximately 6 million patients per year, with a high economic impact. To exacerbate the problem, these wounds render the individual susceptible to life-threatening microbial infections. Because current therapeutic strategies have proved suboptimal, it is imperative to focus on new therapeutic approaches and the development of technologies for both short- and long-term wound management. In recent years, nitric oxide (NO) has emerged as a critical molecule in wound healing, with NO levels increasing rapidly after skin damage and gradually decreasing as the healing process progresses. In this study, we examined the effects of a novel NO-releasing nanoparticle technology on wound healing in mice. The results show that the NO nanoparticles (NO-np) significantly accelerated wound healing. NO-np modified leukocyte migration and increased tumor growth factor-β production in the wound area, which subsequently promoted angiogenesis to enhance the healing process. By using human dermal fibroblasts, we demonstrate that NO-np increased fibroblast migration and collagen deposition in wounded tissue. Together, these data show that NO-releasing nanoparticles have the ability to modulate and accelerate wound healing in a pleiotropic manner.
Department of Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, New York, USA.
George
G
Han
Long N
LN
Nguyen
Chitralekha
C
Macherla
Yuling
Y
Chi
Joel M
JM
Friedman
Joshua D
JD
Nosanchuk
Luis R
LR
Martinez
D000279:Administration, Cutaneous; D000818:Animals; D002465:Cell Movement / Q000187:drug effects; D002478:Cells, Cultured; D003094:Collagen / Q000378:metabolism*; D016503:Drug Delivery Systems / Q000379:methods*; D004353:Drug Evaluation, Preclinical / Q000379:methods; D005260:Female; D005347:Fibroblasts / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D051379:Mice; D008807:Mice, Inbred BALB C; D053758:Nanoparticles; D018919:Neovascularization, Physiologic / Q000187:drug effects; D020556:Neutrophil Infiltration / Q000187:drug effects; D009569:Nitric Oxide / Q000008:administration & dosage* / Q000096:biosynthesis / Q000494:pharmacology; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction / Q000379:methods; D012867:Skin / Q000098:blood supply / Q000293:injuries / Q000378:metabolism / Q000473:pathology; D014945:Wound Healing / Q000187:drug effects* / Q000502:physiology
D009569:Nitric Oxide; D003094:Collagen; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse