scholarly journals Estrogen Accelerates Cutaneous Wound Healing by Promoting Proliferation of Epidermal Keratinocytes via Erk/Akt Signaling Pathway

2016 ◽  
Vol 38 (3) ◽  
pp. 959-968 ◽  
Author(s):  
Tao Zhou ◽  
Zicheng Yang ◽  
Yajie Chen ◽  
Yu Chen ◽  
Zongwei Huang ◽  
...  
Keyword(s):  
Wound Healing ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
S Phase ◽  
Epidermal Keratinocytes ◽  
Hacat Cells ◽  
Cutaneous Wound Healing ◽  
Akt Signaling Pathway ◽  
Cutaneous Wound ◽  
Akt Activation

Background: Previous studies have established that estrogen is capable of accelerating cutaneous wound healing through multiple mechanisms, one of which involves affecting keratinocytes biological properties, such as migration, proliferation, etc. This study aims to reveal the underlying molecular mechanisms of estrogen promoting epidermal keratinocytes proliferation. Method & Results: We found that compared with female mice with a normal estrous cycle, female mice with their ovaries removed before puberty exhibited a delayed cutaneous wound healing, thinner epidermis, and significantly fewer proliferating cell nuclear antigen (PCNA)-positive keratinocytes. Moreover, a significant increase in HaCaT proliferation was detected by a CCK8 assay when treated with 17 β-estradiol compared with those treated with control vehicle. Consistent with the results of the CCK8 assay, flow cytometry indicated a high proportion of 17 β-estradiol-treated HaCaT cells in S phase compared with vehicle-treated cells. Western blot analysis demonstrated the activation of Akt, Erk and upregulation of PCNA in HaCaT cells treated with 17 β-estradiol. Interestingly, Erk activation occurred prior to Akt activation. Upregulation of PCNA expression, elevated proliferation and high S phase fraction of HaCaT cell by 17 β-estradiol could be reversed by an Akt or Erk inhibitor. Moreover, Erk inhibition reversed 17 β-estradiol-induced Akt activation, whereas an Akt inhibitor exhibited no effect on Erk, further suggesting that Erk was on the upstream while Akt on the downstream of the signaling pathway. Conclusion: This study demonstrates that one of the critical mechanisms underlying 17 β-estradiol promoting skin wound healing is through regulation of keratinocyte proliferation via Erk/Akt signaling pathway.

scholarly journals MicroRNA-26a inhibits wound healing through decreased keratinocytes migration by regulating ITGA5 through PI3K/AKT signaling pathway

2020 ◽  
Vol 40 (9) ◽  
Author(s):  
Zhongping Jiang ◽  
Jie Wei ◽  
Weize Yang ◽  
Wen Li ◽  
Feng Liu ◽  
...  
Keyword(s):  
Wound Healing ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Luciferase Reporter ◽  
Epidermal Keratinocytes ◽  
Dependent Manner ◽  
Hacat Cells ◽  
Akt Signaling Pathway ◽  
Tgf Β1

Abstract Background: Keratinocyte migration is essential for skin wound healing and recent studies demonstrated that microRNAs (miRNAs) are involved in the differentiation, migration and apoptosis in keratinocytes. However, the function of miR-26a in wound healing remains to be largely explored. Methods: Northern blot and quantitative reverse transcriptase PCR (qRT-PCR) were used to detect the miR-26a expression and Western blot was used to detect integrin α-5 (ITGA5), phosphatidylinositol-3-kinase (PI3K), p-PI3K, protein kinase B (AKT) and p-AKT protein expression in immortalized human keratinocyte cell line HaCaT and normal human epidermal keratinocytes (NHEK) after 2 ng/ml transforming growth factor-β1 (TGF-β1) treatment for 0, 6, 12 and 24 h. Transwell assay and Wound healing assay were introduced to measure the cell migration of HaCaT cells. TargetScan online database, luciferase reporter assay and RNA immunoprecipitation (RIP) were employed to confirm the relationship between miR-26a and ITGA5. Results: The RNA expression of miR-26a was down-regulated and ITGA5 protein expression was up-regulated by TGF-β1 treatment in HaCaT and NHEK cells in a time-dependent manner. MiR-26a overexpression inhibited the migration of HaCaT cells induced by TGF-β1 while miR-26a inhibitor enhanced the migration. ITGA5 was a downstream target mRNA and regulated by miR-26a. ITGA5 overexpression reversed the inhibitory effect of miR-26a on migration in HaCaT, while ITGA5 knockdown attenuated the stimulative effect of miR-26a inhibitor in HaCaT via PI3K/AKT signaling pathway. Conclusion: MiR-26a overexpression inhibited TGF-β1 induced HaCaT cells migration via down-regulating ITGA5 through activating the PI3K/AKT signaling pathway.

In vivo cooperation between Bcl‐x L and the phosphoinositide 3‐kinase‐Akt signaling pathway for the protection of epidermal keratinocytes from apoptosis

2003 ◽  
Vol 17 (6) ◽  
pp. 610-620 ◽  
Author(s):  
Jiro Umeda ◽  
Shigetoshi Sano ◽  
Kazuhiko Kogawa ◽  
Noboru Motoyama ◽  
Kunihiko Yoshikawa ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Akt Signaling ◽  
Epidermal Keratinocytes ◽  
Akt Signaling Pathway ◽  
Phosphoinositide 3 Kinase

scholarly journals Sodium humate accelerates cutaneous wound healing by activating TGF-β/Smads signaling pathway in rats

2016 ◽  
Vol 6 (2) ◽  
pp. 132-140 ◽  
Author(s):  
Yuanyuan Ji ◽  
Aijun Zhang ◽  
Xiaobin Chen ◽  
Xiaoxia Che ◽  
Kai Zhou ◽  
...  
Keyword(s):  
Wound Healing ◽  
Signaling Pathway ◽  
Cutaneous Wound Healing ◽  
Cutaneous Wound ◽  
Sodium Humate

Activin B Promotes BMSC-Mediated Cutaneous Wound Healing by Regulating Cell Migration via the JNK—ERK Signaling Pathway

2014 ◽  
Vol 23 (9) ◽  
pp. 1061-1073 ◽  
Author(s):  
Min Zhang ◽  
Li Sun ◽  
Xueer Wang ◽  
Shixuan Chen ◽  
Yanan Kong ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Signaling Pathway ◽  
Erk Signaling ◽  
Cutaneous Wound Healing ◽  
Cutaneous Wound

scholarly journals Exosomes Derived from Dental Pulp Stem Cells Accelerate Cutaneous wound Healing by Enhancing Angiogenesis via Cdc42/p38 MAPK Pathway

2021 ◽  
Author(s):  
Ziyu Zhou ◽  
Jianmao Zheng ◽  
Danle Lin ◽  
Yanan Chen ◽  
Xiaoli Hu
Keyword(s):  
Stem Cells ◽  
Wound Healing ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Dental Pulp ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Cutaneous Wound Healing ◽  
Cutaneous Wound ◽  
Protein Levels

Abstract Background: Skin wound healing is a common challenging clinical problem and need advanced treatment strategies. Here, we investigated the therapeutic effects of exosomes derived from dental pulp stem cells (DPSC-Exos) on cutaneous wound healing and the underlying mechanisms. Methods: The effects of DPSC-Exos on cutaneous wound healing in mice were examined by measuring wound closure rates, histological and immunohistochemical analysis. A series of functional assays were performed to evaluate the effects of DPSC-Exos on the angiogenic activities of human umbilical vein endothelial cells (HUVECs) in vitro. TMT-based quantitative proteomic analysis of DPSCs and DPSC-Exos was performed. Gene ontology (GO) and KEGG pathway enrichment analysis were used to evaluate biological functions and pathways for the differentially expressed proteins in DPSC-Exos. Western blot was used to assess the protein levels of Cdc42 and p38 in DPSC-Exos-induced angiogenesis of HUVECs. SB203580, a p38 MAPK signaling pathway inhibitor, was employed to verify the role of p38 MAPK pathway in these processes.Results: Histological and immunohistochemical staining revealed that DPSC-Exos accelerated wound healing by improving neovascularization. DPSC-Exos augmented the migration, proliferation, and capillary formation capacity of HUVECs. Proteomic data demonstrated that proteins contained in DPSC-Exos regulated vasculature development and angiogenesis. Pathway analysis showed that proteins expressed in DPSC-Exos were involved in several pathways including MAPK pathway. Western blotting demonstrated that DPSC-Exos increased the protein levels of Cdc42 and phosphorylation of p38 in HUVECs. SB203580 suppressed the angiogenesis of HUVECs induced by DPSC-Exos.Conclusions: DPSC-Exos could accelerate cutaneous wound healing by enhancing the angiogenic properties of HUVECs via Cdc42/p38 MAPK signaling pathway.

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