miRNA in wound inflammation and angiogenesis.
Chronic wounds represent a rising health and economic burden to our society. Emerging studies indicate that miRNAs play a key role in regulating several hubs that orchestrate the wound inflammation and angiogenesis processes. Of interest to wound inflammation are the regulatory loops where inflammatory mediators elicited following injury are regulated by miRNAs, as well as regulate miRNA expression. Adequate angiogenesis is a key determinant of success in ischemic wound repair. Hypoxia and cellular redox state are among the key factors that drive wound angiogenesis. We provided first evidence demonstrating that miRNAs regulate cellular redox environment via a NADPH oxidase-dependent mechanism in human microvascular endothelial cells (HMECs). We further demonstrated that hypoxia-sensitive miR-200b is involved in induction of angiogenesis by directly targeting Ets-1 in HMECs. These studies point toward a potential role of miRNA in wound angiogenesis. miRNA-based therapeutics represent one of the major commercial hot spots in today's biotechnology market space. Understanding the significance of miRs in wound inflammation and angiogenesis may help design therapeutic strategies for management of chronic nonhealing wounds.
Department of Surgery, The Ohio State University Medical Center, Columbus, Ohio 43210, USA. sashwati.roy@osumc.edu
Sashwati
S
Roy
Chandan K
CK
Sen
D000818:Animals; D018932:Chemokine CCL2 / Q000235:genetics / Q000502:physiology; D005786:Gene Expression Regulation; D006801:Humans; D000860:Hypoxia / Q000235:genetics / Q000503:physiopathology; D007249:Inflammation / Q000235:genetics* / Q000503:physiopathology*; D035683:MicroRNAs / Q000235:genetics* / Q000502:physiology* / Q000627:therapeutic use; D008954:Models, Biological; D019255:NADPH Oxidases / Q000378:metabolism; D018919:Neovascularization, Physiologic / Q000235:genetics*; D010084:Oxidation-Reduction; D051193:Toll-Like Receptors / Q000235:genetics / Q000502:physiology; D014945:Wound Healing / Q000235:genetics / Q000502:physiology; D014947:Wounds and Injuries / Q000235:genetics* / Q000503:physiopathology*
D018932:Chemokine CCL2; D035683:MicroRNAs; D051193:Toll-Like Receptors; D019255:NADPH Oxidases