Neuroanatomy of the Cutaneous Nervous System Regarding Wound Healing

Author(s):  
Shealinna Ge ◽  
Amor Khachemoune

Wound healing is an important topic in modern medicine across many disciplines. Healing of all cutaneous wounds, whether accidentally sustained or intentionally created, requires the common yet complex set of interactions between the immune, circulatory, nervous, endocrine, and integumentary systems. Deficits in any of these systems or the molecular factors that mediate their communications can contribute to impaired healing of cutaneous wounds. While the stages of wound repair, angiogenesis, growth factors, and cytokines involved have been extensively studied, the role of the cutaneous nervous system in wound healing has not been well outlined. We have provided a basic overview of cutaneous innervation and wound repair for the dermatologic surgeon by outlining the normal cutaneous nervous anatomy and function and discussing the most important neuropeptides that mediate the wound healing process.

2018 ◽  
Vol 32 (8) ◽  
pp. 1011-1023 ◽  
Author(s):  
Ji-Ung Park ◽  
Seol-Ha Jeong ◽  
Eun-Ho Song ◽  
Juha Song ◽  
Hyoun-Ee Kim ◽  
...  

In this study, we evaluated the surface characterization of a novel chitosan–silica hybridized membrane and highlighted the substantial role of silica in the wound environment. The chemical coupling of chitosan and silica resulted in a more condensed network compared with pure chitosan, which was eventually able to stably maintain its framework, particularly in the wet state. In addition, we closely observed the wound-healing process along with the surface interaction between chitosan–silica and the wound site using large-surface-area wounds in a porcine model. Our evidence indicates that chitosan–silica exerts a synergetic effect of both materials to promote a remarkable wound-healing process. In particular, the silica in chitosan–silica accelerated wound closure including wound contraction, and re-epithelialization via enhancement of cell recruitment, epidermal maturity, neovascularization, and granulation tissue formation compared with pure chitosan and other commercial dressing materials. This advanced wound dressing material may lead to effective treatment for problematic cutaneous wounds and can be further applied for human skin regeneration.


2020 ◽  
Vol 21 (2) ◽  
pp. 521
Author(s):  
Chen ◽  
Chen ◽  
Simões ◽  
Wu ◽  
Dai ◽  
...  

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.


Author(s):  
Shealinna Ge ◽  
Amor Khachemoune

The skin is a neuroimmunoendocrine organ that regularly undergoes injury and repair. The complex process of wound healing relies heavily on the cutaneous nervous system. Despite the observation that wound healing deficiencies cause significant morbidity and mortality for patients with nervous dysfunction across many disciplinaries, the role of cutaneous innervation in wound repair has not been well elucidated. In a previous article, we learned the basics of cutaneous neuroanatomy and the important neuropeptides involved in the wound healing process. Currently, we aim to synthesize the basics with observations from animal models and human studies for a more comprehensive understanding of nervous system involvement in cutaneous wound healing. We have demonstrated in this review, the importance of the cutaneous nervous system in each phase of wound healing through basic science research, animal experiments, and human studies.


Molecules ◽  
2021 ◽  
Vol 26 (9) ◽  
pp. 2424
Author(s):  
Ipek Süntar ◽  
Sümeyra Çetinkaya ◽  
Emiliano Panieri ◽  
Sarmistha Saha ◽  
Brigitta Buttari ◽  
...  

Wound healing involves a series of cellular events in damaged cells and tissues initiated with hemostasis and finally culminating with the formation of a fibrin clot. However, delay in the normal wound healing process during pathological conditions due to reactive oxygen species, inflammation and immune suppression at the wound site represents a medical challenge. So far, many therapeutic strategies have been developed to improve cellular homeostasis and chronic wounds in order to accelerate wound repair. In this context, the role of Nuclear factor erythroid 2-related factor 2 (Nrf2) during the wound healing process has been a stimulating research topic for therapeutic perspectives. Nrf2 is the main regulator of intracellular redox homeostasis. It increases cytoprotective gene expression and the antioxidant capacity of mammalian cells. It has been reported that some bioactive compounds attenuate cellular stress and thus accelerate cell proliferation, neovascularization and repair of damaged tissues by promoting Nrf2 activation. This review highlights the importance of the Nrf2 signaling pathway in wound healing strategies and the role of bioactive compounds that support wound repair through the modulation of this crucial transcription factor.


2021 ◽  
Vol 165 ◽  
pp. 39
Author(s):  
Francesca Lombardi ◽  
Silvano Santini ◽  
Paola Palumbo ◽  
Valeria Cordone ◽  
Virginio Bignotti ◽  
...  

Author(s):  
Ahmed G. Hegazi ◽  
Faiz M. Al Guthami ◽  
Mohamed H. Basiouny ◽  
Ahmed F.M. Al Gethami

Honey has been documented as the oldest traditional medicine. It has been effective in suppressing inflammation, wound repair enhancer, and rapid autolytic debridement. The aim of this investigation was to evaluate the role of Saudi Arabia Talh honey (Acacia nilotica) dressing as a good alternative in care of diabetic foot (DFU) healing activity for twenty patients, wound total bacterial count, and serum cytokines levels (IFN-γ, IL-1, and IL-6). The results showed that Talh honey stimulates the wound healing process, broad-spectrum antibacterial activity, and reduction in the proinflammatory cytokines IFN-γ, IL-1, and IL-6 levels. It could be concluded that Talh honey bioactivities enhance wound healing by promoting tissue growth leading to wound repair, antibacterial, and reduction of inflammation.


2020 ◽  
Author(s):  
Daisuke Ito ◽  
Hiroyasu Ito ◽  
Takayasu Ideta ◽  
Ayumu Kanbe ◽  
Soranobu Ninomiya ◽  
...  

Abstract Background The skin wound healing process is regulated by various cytokines, chemokines, and growth factors. Recent reports have demonstrated that spermine/spermidine (SPD) promote wound healing through urokinase-type plasminogen activator (uPA)/uPA receptor (uPAR) signaling in vitro. Here, we investigated whether the systemic and topical administration of SPD would accelerate the skin wound-repair process in vivo.Methods A skin wound repair model was established using C57BL/6 J mice. SPD was mixed with white petrolatum for topical administration. For systemic administration, SPD mixed with drinking water was orally administered. Changes in wound size over time were calculated using digital photography.Results Systemic and topical SPD treatment significantly accelerated skin wound healing. The administration of SPD promoted the uPA/uPAR pathway in wound sites. Moreover, topical treatment with SPD enhanced the expression of IL-6 and TNF-α in wound sites. Scratch and cell proliferation assays revealed that SPD administration accelerated scratch wound closure and cell proliferation in vitro.Conclusion These results indicate that treatment with SPD promotes skin wound healing through activation of the uPA/uPAR pathway and induction of the inflammatory response in wound sites. The administration of SPD might contribute to new effective treatments to accelerate skin wound healing.


2021 ◽  
Author(s):  
Mary Yinghua Zhang ◽  
Shuyi Fang ◽  
Hongyu Gao ◽  
Xiaoli Zhang ◽  
Dongsheng Gu ◽  
...  

ABSTRACTWe report our discovery of an important player in the development of skin fibrosis, a hallmark of scleroderma. Scleroderma is a fibrotic disease, affecting 70,000 to 150,000 Americans. Fibrosis is a pathological wound healing process that produces an excessive extracellular matrix to interfere with normal organ function. Fibrosis contributes to nearly half of human mortality. Scleroderma has heterogeneous phenotypes, unpredictable outcomes, no validated biomarkers, and no effective treatment. Thus, strategies to slow down scleroderma progression represent an urgent medical need. While a pathological wound healing process like fibrosis leaves scars and weakens organ function, oral mucosa wound healing is a scarless process. After re-analyses of gene expression datasets from oral mucosa wound healing and skin fibrosis, we discovered that several pathways constitutively activated in skin fibrosis are transiently induced during oral mucosa wound healing process, particularly the amphiregulin (Areg) gene. Areg expression is upregulated ~10 folds 24hrs after oral mucosa wound but reduced to the basal level 3 days later. During bleomycin-induced skin fibrosis, a commonly used mouse model for skin fibrosis, Areg is up-regulated throughout the fibrogenesis and is associated with elevated cell proliferation in the dermis. To demonstrate the role of Areg for skin fibrosis, we used mice with Areg knockout, and found that Areg deficiency essentially prevents bleomycin-induced skin fibrosis. We further determined that bleomycin-induced cell proliferation in the dermis was not observed in the Areg null mice. Furthermore, we found that inhibiting MEK, a downstream signaling effector of Areg, by selumetinib also effectively blocked bleomycin-based skin fibrosis model. Based on these results, we concluded that the Areg-EGFR-MEK signaling axis is critical for skin fibrosis development. Blocking this signaling axis may be effective in treating scleroderma.


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