scholarly journals MicroRNA-485-5p reduces keratinocyte proliferation and migration by regulating ITGA5 expression in skin wound healing

2021 ◽  
Vol 19 (12) ◽  
pp. 2553-2557
Author(s):  
Keyu Yuan ◽  
Yi Sun ◽  
Yu Ji
Keyword(s):  
Wound Healing ◽  
Cell Viability ◽  
Skin Wound ◽  
Hacat Cells ◽  
Skin Wound Healing ◽  
Keratinocyte Proliferation ◽  
Downstream Target ◽  
And Migration ◽  
Tgf Β1 ◽  
Proliferation And Migration

Purpose: To determine the effect of miR-485-5p on keratinocyte proliferation and migration.Methods: Human primary keratinocytes (HaCaT cells) were treated with different concentrations of transforming growth factor-β1 (TGF)-β1. miR-485-5p expression levels were determined using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). MTT (3-[4,5-dimethylthiazol-2- yl]-2,5 diphenyl tetrazolium bromide) and wound healing assays were performed to investigate the regulatory effects of miR-485-5p on cell viability and migration of HaCaT cells. Downstream target gene expression of miR-485-5p was determined using a luciferase activity assay.Results: In HaCaT cells, miR-485-5p was time- and dose-dependently downregulated by TGF-β1 treatment (p < 0.05). Forced expression of miR-485-5p decreased cell viability and migration of HaCaT cells (p < 0.05). Knockdown of miR-485-5p enhanced HaCaT cell viability and migration. Integrin subunit alpha-5 (ITGA5) was predicted and verified to be a downstream target of miR-485-5p in HaCaT cells. Overexpression of ITGA5 attenuated the miR-485-5p-induced decrease of HaCaT cell viability and migration (p < 0.05).Conclusion: MiR-485-5p reduces cell proliferation and migration of keratinocytes through the regulation of ITGA5. This mechanism provides a potential therapeutic strategy for skin wound healing. Keywords: ITGA5, Keratinocyte, Cell migration, MiR-485-5p, Cell proliferation, Wound healing

scholarly journals MicroRNA-31 Promotes Skin Wound Healing by Enhancing Keratinocyte Proliferation and Migration

2015 ◽  
Vol 135 (6) ◽  
pp. 1676-1685 ◽  
Author(s):  
Dongqing Li ◽  
X.I. Li ◽  
Aoxue Wang ◽  
Florian Meisgen ◽  
Andor Pivarcsi ◽  
...  
Keyword(s):  
Wound Healing ◽  
Skin Wound ◽  
Skin Wound Healing ◽  
Keratinocyte Proliferation ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Puerarin Improves Dexamethasone-Impaired Wound Healing In Vitro and In Vivo by Enhancing Keratinocyte Proliferation and Migration

2021 ◽  
Vol 11 (19) ◽  
pp. 9343
Author(s):  
Ly Thi Huong Nguyen ◽  
Sang-Hyun Ahn ◽  
Min-Jin Choi ◽  
In-Jun Yang ◽  
Heung-Mook Shin
Keyword(s):  
Wound Healing ◽  
Healing Process ◽  
Wound Healing Process ◽  
Hacat Cells ◽  
Impaired Wound Healing ◽  
Keratinocyte Proliferation ◽  
And Migration ◽  
Proliferation And Migration

The delayed and impaired wound healing caused by dexamethasone (DEX) is commonly reported. Puerarin, the major isoflavone found in Pueraria montana var. lobata (Willd.) Sanjappa & Pradeep promoted the wound healing process in diabetic rats. However, the effects and underlying mechanisms of puerarin on DEX-impaired wound healing have not been investigated. This study examined the potential uses of puerarin in upregulating keratinocyte proliferation and migration in dexamethasone (DEX)-suppressed wound healing model. The effects of puerarin on wound healing in vivo were investigated by taking full-thickness 5 mm punch biopsies from the dorsal skin of BALB/c mice and then treating them topically with 0.1% DEX. For the in vitro study, DEX-treated HaCaT cells were used to examine the effects of puerarin on DEX-induced keratinocyte proliferation and migration and the mechanisms of its action. Puerarin, when applied topically, accelerated the wound closure rate, increased the density of the capillaries, and upregulated the level of collagen fibers and TGF-β in the wound sites compared to the DEX-treated mice. Puerarin promoted the proliferation and migration of keratinocytes by activating the ERK and Akt signaling pathways in DEX-treated HaCaT cells. In conclusion, puerarin could be effective in reversing delayed and disrupted wound healing associated with DEX treatments.

scholarly journals Photodynamic therapy accelerates skin wound healing through promoting re-epithelialization

2021 ◽  
Vol 9 ◽  
Author(s):  
Zengjun Yang ◽  
Xiaohong Hu ◽  
Lina Zhou ◽  
Yaxiong He ◽  
Xiaorong Zhang ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Wound Healing ◽  
Photodynamic Therapy ◽  
Skin Wound ◽  
Hair Follicles ◽  
Skin Wound Healing ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Epidermal stem cells (EpSCs) that reside in cutaneous hair follicles and the basal layer of the epidermis are indispensable for wound healing and skin homeostasis. Little is known about the effects of photochemical activation on EpSC differentiation, proliferation and migration during wound healing. The present study aimed to determine the effects of photodynamic therapy (PDT) on wound healing in vivo and in vitro. Methods We created mouse full-thickness skin resection models and applied 5-aminolevulinic acid (ALA) for PDT to the wound beds. Wound healing was analysed by gross evaluation and haematoxylin–eosin staining in vivo. In cultured EpSCs, protein expression was measured using flow cytometry and immunohistochemistry. Cell migration was examined using a scratch model; apoptosis and differentiation were measured using flow cytometry. Results PDT accelerated wound closure by enhancing EpSC differentiation, proliferation and migration, thereby promoting re-epithelialization and angiogenesis. PDT inhibited inflammatory infiltration and expression of proinflammatory cytokines, whereas the secretion of growth factors was greater than in other groups. The proportion of transient amplifying cells was significantly greater in vivo and in vitro in the PDT groups. EpSC migration was markedly enhanced after ALA-induced PDT. Conclusions Topical ALA-induced PDT stimulates wound healing by enhancing re-epithelialization, promoting angiogenesis as well as modulating skin homeostasis. This work provides a preliminary theoretical foundation for the clinical administration of topical ALA-induced PDT in skin wound healing.

scholarly journals Preliminary Study on Human Adipose Stem Cells Promoting Skin Wound Healing Through Notch1 Signaling Pathway

2022 ◽  
Author(s):  
Yi Wang ◽  
Qinchao Wu ◽  
Yang Zheng ◽  
Chao Wang ◽  
Xu Ding ◽  
...  
Keyword(s):  
Stem Cells ◽  
Wound Healing ◽  
Signaling Pathway ◽  
Skin Wound ◽  
Hacat Cells ◽  
Skin Wound Healing ◽  
Notch1 Signaling ◽  
And Migration ◽  
Notch1 Signaling Pathway ◽  
Human Adipose Stem Cells

Abstract Background: Mesenchymal stem cells (MSCs) have been documented as possible candidates for wound healing treatment because their use could reinforce the regenerative capacity of many tissues. Human adipose stem cells (hADSCs) have the advantages of easy access, large quantity and easy operation. They can be fully applied in the treatment of skin wounds. In this study, we aim to explore the roles and potential mechanisms of hADSCs in cutaneous wound healing.Methods: hADSCs were obtained from human subcutaneous fat. Adipocytes and osteocytes differentiated from hADSCs were determined by staining with Oil Red O and alkaline phosphatase (ALP), respectively. We assessed the effects of hADSCs and hADSC conditional medium (CM) on wound healing in an injury model of mice. Than, we investigated the biological effects of hADSCs on human keratinocytes HaCAT cells in vitro.Results: The results showed that hADSCs could be successfully differentiated into osteogenic and lipogenic cells. hADSCs and hADSCs-CM significantly promote skin wound healing in vivo. hADSCs significantly promoted HaCAT cells proliferation and migration through activating Notch1 signaling pathway, and activated the AKT signaling pathway by Rps6kb1 kinase in HaCAT cells. In addition, we found that hADSCs-mediated activation of Rps6kb1/AKT signaling was dependent on the Notch1 signaling pathway.Conclusion: We demonstrated that hADSCs can promote skin cell-HaCAT cells proliferation and migration via Notch1 pathway, suggesting that hADSCs may provide an alternative therapeutic approach for the treatment of skin injury.

scholarly journals Impaired skin wound healing in peroxisome proliferator–activated receptor (PPAR)α and PPARβ mutant mice

2001 ◽  
Vol 154 (4) ◽  
pp. 799-814 ◽  
Author(s):  
Liliane Michalik ◽  
Béatrice Desvergne ◽  
Nguan Soon Tan ◽  
Sharmila Basu-Modak ◽  
Pascal Escher ◽  
...  
Keyword(s):  
Wound Healing ◽  
Skin Wound ◽  
Mutant Mice ◽  
Peroxisome Proliferator ◽  
Skin Wound Healing ◽  
Peroxisome Proliferator Activated Receptor ◽  
Keratinocyte Proliferation ◽  
Tetradecanoylphorbol Acetate ◽  
Proliferation And Differentiation ◽  
And Migration

We show here that the α, β, and γ isotypes of peroxisome proliferator–activated receptor (PPAR) are expressed in the mouse epidermis during fetal development and that they disappear progressively from the interfollicular epithelium after birth. Interestingly, PPARα and β expression is reactivated in the adult epidermis after various stimuli, resulting in keratinocyte proliferation and differentiation such as tetradecanoylphorbol acetate topical application, hair plucking, or skin wound healing. Using PPARα, β, and γ mutant mice, we demonstrate that PPARα and β are important for the rapid epithelialization of a skin wound and that each of them plays a specific role in this process. PPARα is mainly involved in the early inflammation phase of the healing, whereas PPARβ is implicated in the control of keratinocyte proliferation. In addition and very interestingly, PPARβ mutant primary keratinocytes show impaired adhesion and migration properties. Thus, the findings presented here reveal unpredicted roles for PPARα and β in adult mouse epidermal repair.

scholarly journals Overexpression of the Oral Mucosa-Specific microRNA-31 Promotes Skin Wound Closure

2019 ◽  
Vol 20 (15) ◽  
pp. 3679 ◽  
Author(s):  
Lin Chen ◽  
Alyne Simões ◽  
Zujian Chen ◽  
Yan Zhao ◽  
Xinming Wu ◽  
...  
Keyword(s):  
Wound Healing ◽  
Oral Mucosa ◽  
Wound Closure ◽  
Expression Patterns ◽  
Skin Wound ◽  
Skin Wound Healing ◽  
Specific Expression ◽  
Keratinocyte Proliferation

Wounds within the oral mucosa are known to heal more rapidly than skin wounds. Recent studies suggest that differences in the microRNAome profiles may underlie the exceptional healing that occurs in oral mucosa. Here, we test whether skin wound-healing can be accelerating by increasing the levels of oral mucosa-specific microRNAs. A panel of 57 differentially expressed high expresser microRNAs were identified based on our previously published miR-seq dataset of paired skin and oral mucosal wound-healing [Sci. Rep. (2019) 9:7160]. These microRNAs were further grouped into 5 clusters based on their expression patterns, and their differential expression was confirmed by TaqMan-based quantification of LCM-captured epithelial cells from the wound edges. Of these 5 clusters, Cluster IV (consisting of 8 microRNAs, including miR-31) is most intriguing due to its tissue-specific expression pattern and temporal changes during wound-healing. The in vitro functional assays show that ectopic transfection of miR-31 consistently enhanced keratinocyte proliferation and migration. In vivo, miR-31 mimic treatment led to a statistically significant acceleration of wound closure. Our results demonstrate that wound-healing can be enhanced in skin through the overexpression of microRNAs that are highly expressed in the privileged healing response of the oral mucosa.

scholarly journals Growth Differentiation Factor-9 Promotes Fibroblast Proliferation and Migration in Keloids through the Smad2/3 Pathway

2016 ◽  
Vol 40 (1-2) ◽  
pp. 207-218 ◽  
Author(s):  
Zhaohua Jiang ◽  
Qingxiong Yu ◽  
Lingling Xia ◽  
Yi Zhang ◽  
Xiuxia Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Wound Healing ◽  
Growth Factor ◽  
Fibroblast Proliferation ◽  
Differentiation Factor ◽  
Cox 2 ◽  
And Migration ◽  
Tgf Β1 ◽  
Keloid Fibroblasts ◽  
Proliferation And Migration

Background: Keloids are fibroproliferative scars that develop as a result of a dysregulated wound healing process; however, the molecular mechanisms of keloid pathogenesis remain unclear. Keloids are characterized by the ability to spread beyond the original boundary of the wound, and they represent a significant clinical challenge. Previous work from our group suggested that growth differentiation factor (GDF)-9 plays a role in the invasive behavior of keloids. Here, we examined the involvement of GDF-9 in keloid formation and spread and elucidated a potential underlying mechanism. Methods: The expression of GDF-9, cyclooxygenase (COX)-2, vascular epidermal growth factor (VEGF)-C, matrix metalloprotease (MMP)-2, MMP-9, transforming growth factor (TGF)-β1, and the related signaling pathway components in human keloid tissues or keloid fibroblasts (kFBs) was monitored by qRT-PCR and western blot. A series of overexpression and silencing experiments in normal and keloid fibroblasts were used to modify the expression of GDF-9. The effects of GDF-9 on kFB proliferation and migration were assessed using the CCK-8, cell cycle and scratch wound healing assays. Results: GDF-9 promotes fibroblast proliferation and migration. GDF-9 silencing in kFBs decreased cell proliferation, blocked cell cycle progression, downregulated the angiogenic markers COX-2 and VEGF-C, and downregulated MMP-2 and MMP-9 expression, whereas it had no effect on the levels of TGF-β1. GDF-9 silencing significantly inhibited Smad2 and Smad3 phosphorylation in kFBs. Conclusions: GDF-9 promotes the proliferation and migration of kFBs via a mechanism involving the Smad2/3 pathway.

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