Abstract
The oral mucosa exhibits exceptional healing capability when compared to skin. Recent studies suggest that intrinsic differences in coding genes and regulatory small non-coding RNA (sncRNA) genes (e.g., microRNAs) may underlie the exceptional healing that occurs in the oral mucosa. Here, we investigate the role of a novel class of sncRNA—Piwi-interacting RNA (piRNA)—in the tissue-specific differential response to injury. An abundance of piRNAs was detected in both skin and oral mucosal epithelium during wound healing. The expression of PIWI genes (the obligate binding partners of piRNAs) was also detected in skin and oral wound healing. This data suggested that PIWI-piRNA machinery may serve an unknown function in the highly orchestrated wound healing process. Furthermore, unique tissue-specific piRNA profiles were obtained in the skin and oral mucosal epithelium, and substantially more changes in piRNA expression were observed during skin wound healing than oral mucosal wound healing. Thus, we present the first clue suggesting a role of piRNA in wound healing, and provide the first site-specific piRNA profile of skin and oral mucosal wound healing. These results serve as a foundation for the future investigation of the functional contribution(s) of piRNA in wound repair and tissue regeneration.
Highlights
IntroductionImpaired cutaneous wound healing affects approximately 6.7 million patients in the U.S, and up to 2% of the population in developed countries suffer from chronic wounds [1]
Recent comparative studies focusing on differential molecular characterization of the skin and oral mucosa have revealed that the intrinsic molecular differences in skin and oral mucosa contribute to the divergent wound healing outcomes [2,3,4]
Extensive studies on the roles of piwi-interacting RNA (piRNA) in the germline and gonads revealed that piRNAs exert their functions by forming RNA-induced silencing complex (RISC) with PIWI proteins [10,11]
Summary
Impaired cutaneous wound healing affects approximately 6.7 million patients in the U.S, and up to 2% of the population in developed countries suffer from chronic wounds [1]. Recent comparative studies focusing on differential molecular characterization of the skin and oral mucosa have revealed that the intrinsic molecular differences in skin and oral mucosa contribute to the divergent wound healing outcomes [2,3,4]. This novel approach defines critical molecular regulators involved in accelerated wound healing and allows the harnessing of regenerative healing capabilities in oral mucosa to treat deficient healing processes. Wound healing is a complex process that consists of four overlapping phases: Hemostasis, Inflammatory, Proliferative, and Maturation This highly orchestrated process is regulated by numerous genetic and epigenetic regulators, including regulatory small non-coding RNAs (sncRNA) such as microRNA and piwi-interacting RNA (piRNA). Our results provide the first clue that piRNA may play an important role in regulating wound healing
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