scholarly journals Alda-1, an Aldehyde Dehydrogenase 2 Agonist, Improves Cutaneous Wound Healing by Activating Epidermal Keratinocytes Via Akt/GSK-3β/β-Catenin Pathway

2021 ◽  
Author(s):  
Xinhang Dong ◽  
Mingzi Zhang ◽  
Xiaolei Jin
Keyword(s):  
Wound Healing ◽  
Aldehyde Dehydrogenase ◽  
Epidermal Keratinocytes ◽  
Cutaneous Wound Healing ◽  
Aldehyde Dehydrogenase 2 ◽  
Cutaneous Wound ◽  
Gsk 3Β

scholarly journals The Dishevelled-binding protein CXXC5 negatively regulates cutaneous wound healing

2015 ◽  
Vol 212 (7) ◽  
pp. 1061-1080 ◽  
Author(s):  
Soung-Hoon Lee ◽  
Mi-Yeon Kim ◽  
Hyun-Yi Kim ◽  
Young-Mi Lee ◽  
Heesu Kim ◽  
...  
Keyword(s):  
Wound Healing ◽  
Negative Feedback ◽  
Critical Role ◽  
Dermal Fibroblasts ◽  
Epidermal Keratinocytes ◽  
Binding Motif ◽  
Cutaneous Wound Healing ◽  
Collagen Production ◽  
Cutaneous Wound

Wnt/β-catenin signaling plays important roles in cutaneous wound healing and dermal fibrosis. However, its regulatory mechanism has not been fully elucidated, and a commercially available wound-healing agent targeting this pathway is desirable but currently unavailable. We found that CXXC-type zinc finger protein 5 (CXXC5) serves as a negative feedback regulator of the Wnt/β-catenin pathway by interacting with the Dishevelled (Dvl) protein. In humans, CXXC5 protein levels were reduced in epidermal keratinocytes and dermal fibroblasts of acute wounds. A differential regulation of β-catenin, α-smooth muscle actin (α-SMA), and collagen I by overexpression and silencing of CXXC5 in vitro indicated a critical role for this factor in myofibroblast differentiation and collagen production. In addition, CXXC5−/− mice exhibited accelerated cutaneous wound healing, as well as enhanced keratin 14 and collagen synthesis. Protein transduction domain (PTD)–Dvl-binding motif (DBM), a competitor peptide blocking CXXC5-Dvl interactions, disrupted this negative feedback loop and activated β-catenin and collagen production in vitro. Co-treatment of skin wounds with PTD-DBM and valproic acid (VPA), a glycogen synthase kinase 3β (GSK3β) inhibitor which activates the Wnt/β-catenin pathway, synergistically accelerated cutaneous wound healing in mice. Together, these data suggest that CXXC5 would represent a potential target for future therapies aimed at improving wound healing.

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.

Study on the Effect of Cerium Oxide Nanocubes on Full-Thickness Cutaneous Wound Healing of Type 2 Diabetic Rats

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 643-P ◽  
Author(s):  
YANFEI HAN ◽  
LINDONG LI ◽  
YANJUN LIU ◽  
YOU WANG ◽  
CHUNHUA YAN ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cerium Oxide ◽  
Diabetic Rats ◽  
Cutaneous Wound Healing ◽  
Full Thickness ◽  
Cutaneous Wound ◽  
Type 2 Diabetic
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