Long non‑coding RNA HOTAIR promotes burn wound healing by regulating epidermal stem cells

Abstract

local transplantation of epidermal stem cells (eScs) exerts a therapeutic effect on burn wounds. However, cell viability can impede their clinical application. HoX antisense intergenic rna (HoTair) is involved in regulating adult tissue stem cells, as well as in developmental patterning and pluripotency. However, little is known about its role in regulating eScs. The present study was performed to investigate the effects of HoTair in the modulation of eScs and wound repair. Firstly, reverse transcription-quantitative Pcr was used to detect the relative expression of HoTair during burn wound healing in mice to determine whether HoTair is associated with wound healing. Subsequently, eScs derived from mouse skin were transfected with a lentiviral vector to overexpress or knockdown HoTair. The effects of HoTair on cell proliferation and differentiation were measured by 5-bromodeoxyuridine and MTT assays, and by assessing nanoG mrna expression. lastly, mice with burns were administered a subcutaneous injection of HoTair-overexpressing eScs. images were captured and histological analyses were performed to evaluate wound healing. The results revealed that the expression of HoTair gradually increased and peaked at day 7 post-burn and maintained at relatively high levels until day 14 post-burn during wound healing. Furthermore, overexpression of HoTair promoted eSc proliferation and maintained the stem cell state in vitro. By contrast, suppression of HoTair inhibited cell proliferation and cell stemness. It was also identified that HoTir-overexpressing eScs accelerated re-epithelialization and facilitated burn wound repair. in conclusion, the present findings confirmed an essential role of HOTAIR in the regulation of eSc proliferation and stemness. Therefore, targeting HoTair in eScs may be a potentially promising therapy for burn wound healing.

Spindle‐Like Zinc Silicate Nanoparticles Accelerating Innervated and Vascularized Skin Burn Wound Healing

“…However, large‐area scars were still visible and no dermal layer began to form in Blank group, indicating that the chronic nonhealing wounds induced by deep second‐degree burns cannot self‐repair in 14 days. [ 31 ] Previous studies proved that the complete healing in deep second‐degree burn wounds model needs to take more than 25 days. [ 32 ] Therefore, H&E staining results demonstrated that PCL+5ZS nanofibrous scaffolds could effectively accelerate the wound healing process and promote re‐epithelialization, exhibiting great potential for promoting burns wound healing.…”

Transcriptomic analysis of human skin wound healing and rejuvenation following ablative fractional laser treatment

“…The ephrin receptor signaling pathway, which is important in wound closure and healing [ 67 ], is strongly activated as early as 1 day post treatment followed by a gradual decrease over the 28-day treatment period. The long non-coding RNA HOTAIR regulatory pathway was also activated following fractional laser treatment as would be required for proper wound healing [ 68 ]. Additionally, the large changes in S100 gene expression at 1 day post fractional laser treatment, along with the rapid induction of gene expression of several inflammatory pathways, confirms a quick immune response to the damage and greatly expands previous histochemical study findings [ 42 – 48 ].…”

Transcriptomic Analysis of Human Skin Wound Healing and Rejuvenation Following Ablative Fractional Laser Treatment

“…The ephrin receptor signaling pathway, which is important in wound closure and healing (Nunan et al, 2015), is strongly activated as early as 1 day post treatment followed by a gradual decrease over the 28-day treatment period. The long non-coding RNA HOTAIR regulatory pathway was also activated following fractional laser treatment as would be required for proper wound healing (Shi et al, 2020). Additionally, the large changes in S100 gene expression at 1 day post fractional laser treatment, along with the rapid induction of gene expression of several inflammatory pathways, confirms a quick immune response to the damage and greatly expands previous histochemical study findings (Prignano et al, 2009;Helbig et al, 2011;Xu et al, 2011;Prignano et al, 2012;Helbig et al, 2009;El-Domyati et al, 2007;Zheng et al, 2014).…”