scholarly journals Ozone oil promotes wound healing by increasing the migration of fibroblasts via PI3K/Akt/mTOR signaling pathway

2017 ◽  
Vol 37 (6) ◽  
Author(s):  
Weirong Xiao ◽  
Hua Tang ◽  
Meng Wu ◽  
Yangying Liao ◽  
Ke Li ◽  
...  
Keyword(s):  
Wound Healing ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Western Blotting ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Skin Injury ◽  
Mesenchymal Transition ◽  
Fibroblast Migration ◽  
Western Blotting Assay

Skin injury affects millions of people via the uncontrolled inflammation and infection. Many cellular components including fibroblasts and signaling pathways such as transforming growth factor-β (TGF-β) were activated to facilitate the wound healing to repair injured tissues. C57BL/6 female mice were divided into control and ozone oil treated groups. Excisional wounds were made on the dorsal skin and the fibroblasts were isolated from granulation tissues. The skin injured mouse model revealed that ozone oil could significantly decrease the wound area and accelerate wound healing compared with control group. QPCR and Western blotting assays showed that ozone oil up-regulated collagen I, α-SMA, and TGF-β1 mRNA and protein levels in fibroblasts. Wound healing assay demonstrated that ozone oil could increase the migration of fibroblasts. Western blotting assay demonstrated that ozone oil increased the epithelial–mesenchymal transition (EMT) process in fibroblasts via up-regulating fibronectin, vimentin, N-cadherin, MMP-2, MMP-9, insulin-like growth factor binding protein (IGFBP)-3, IGFBP5, and IGFBP6, and decreasing epithelial protein E-cadherin and cellular senescence marker p16 expression. Mechanistically, Western blotting assay revealed that ozone oil increased the phosphorylation of PI3K, Akt, and mTOR to regulate the EMT process, while inhibition of PI3K reversed this effect of ozone oil. At last, the results from Cytometric Bead Array (CBA) demonstrated ozone oil significantly decreased the inflammation in fibroblasts. Our results demonstrated that ozone oil facilitated the wound healing via increasing fibroblast migration and EMT process via PI3K/Akt/mTOR signaling pathway in vivo and in vitro. The cellular and molecular mechanisms we found here may provide new therapeutic targets for the treatment of skin injury.

Acemannan accelerates cell proliferation and skin wound healing through AKT/mTOR signaling pathway

2015 ◽  
Vol 79 (2) ◽  
pp. 101-109 ◽  
Author(s):  
Wei Xing ◽  
Wei Guo ◽  
Cun-Hua Zou ◽  
Ting-Ting Fu ◽  
Xiang-Yun Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Signaling Pathway ◽  
Skin Wound ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Skin Wound Healing

scholarly journals MicroRNA-99 Family Targets AKT/mTOR Signaling Pathway in Dermal Wound Healing

PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e64434 ◽  
Author(s):  
Yi Jin ◽  
Stéphanie D. Tymen ◽  
Dan Chen ◽  
Zong Juan Fang ◽  
Yan Zhao ◽  
...  
Keyword(s):  
Wound Healing ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Dermal Wound Healing ◽  
Dermal Wound

DNMT1-mediated lncRNA MEG3 methylation accelerates endothelial-mesenchymal transition in diabetic retinopathy through the PI3K/AKT/mTOR signaling pathway

2020 ◽  
Author(s):  
Yue He ◽  
Yujiao Dan ◽  
Xiaorong Gao ◽  
Li Huang ◽  
Hongbin Lv ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Signaling Pathway ◽  
Dna Methyltransferase ◽  
Cell Model ◽  
Mtor Signaling ◽  
Diabetic Patients ◽  
Cell Models ◽  
Mtor Signaling Pathway ◽  
Mesenchymal Transition ◽  
Endothelial Mesenchymal Transition

Diabetic retinopathy (DR) is one of the serious complications that occur in diabetic patients that frequently causes blindness. Long non-coding RNAs (lncRNAs) have been associated with DR pathology. This study aimed to determine the underlying mechanism of lncRNA maternally expressed gene 3 (MEG3) in association with DNA methyltransferase 1 (DNMT1) in the endothelial-mesenchymal transition (endMT) that occurs in DR. A rat model of DR was induced by streptozotocin (STZ) injection, and high glucose (HG)-induced cell model was established by exposing microvascular endothelial cells obtained from retina of rats to HG. Subsequently, MEG3 was overexpressed in rat and cell models to characterize its impact on endMT in DR and the involvement of the PI3K/AKT/mTOR signaling pathway. Furthermore, the methylation level of MEG3 promoter region was determined with the application of methylation-specific polymerase chain reaction, followed by Chromatin immunoprecipitation assay for methyltransferase enrichment. Finally, we examined the regulation of DNMT1 on MEG3 methylation and endMT in the HG-induced cell model. The results obtained revealed downregulated MEG3 expression in DR rat and cell models. Overexpressed MEG3 was shown to suppress endMT in DR rat and cell models through the inhibition of the PI3K/AKT/mTOR signaling pathway. Notably, DNMT1 could promote MEG3 promoter methylation to inhibit MEG3 expression by recruiting methyltransferase, which activated the PI3K/AKT/mTOR signaling pathway to accelerate endMT in DR. These findings further highlighted the inhibitory effect of MEG3 on endMT in DR, thus presenting a novel therapeutic target candidate for DR treatment.

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