An investigation of crosstalk between Wnt/β-catenin and transforming growth factor-β signaling in androgenetic alopecia

Lu, Gui-Qing; Wu, Z.; Chu, Xiaoyan; Bi, Zhigang; Fan, Wenhong

doi:10.1097/md.0000000000004297

Cited by 38 publications

(28 citation statements)

References 22 publications

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“…Also, this signal has been shown to regulate DPCs inductive properties (11). Wnt/β-catenin has been shown to be the early trigger of DPCs in the induction and initiation of hair follicle formation (12). Together, active agents that induce or enhance stem cell signals and properties of DPCs may benefit the therapeutic treatment of hair loss.…”

mentioning

confidence: 99%

Finasteride Enhances Stem Cell Signals of Human Dermal Papilla Cells

Rattanachitthawat

Pinkhien

Opanasopit

et al. 2019

In Vivo

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Background/Aim: Finasteride (FN) has been widely used to treat androgenetic alopecia (AGA). This study aimed at exploring the effect of FN on DP stem cell properties. Materials and Methods: Effect of FN on stem cell properties was tested in a DP cell line and 2 human primary DP cells (HDPCs1 and HDPCs2). Cell toxicity and growth were analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide (MTT) assay. The aggregation behavior was observed by phase-contrast microscopy and a scanning electron microscope (SEM). Effects of FN on cell signaling were determined by western blotting and immunocytochemistry. Results: Treatment of DPCs with FN was able to significantly increase their aggregation behavior and the expression of stem cell transcription factors Nanog and Sox-2, when compared to the non-treated control. FN up-regulated stem cell regulatory proteins through the activation of protein kinase B (AKT), β-catenin, and integrin-β1. Conclusion: FN had an interesting biological effect on stem cell induction. These findings support the use of this drug for hair loss control and the development of regeneration approaches.

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mentioning

confidence: 99%

Finasteride Enhances Stem Cell Signals of Human Dermal Papilla Cells

Rattanachitthawat

Pinkhien

Opanasopit

et al. 2019

In Vivo

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“…K. Foitzik and X. Liu with their colleagues determined on an animal model that TGF-β1 inhibits hair growth by shortening anagen and initiating follicle catagen. The dependence of TGF-β1 expression on the hair follicle phase was also shown (Foitzik et al, 2000;Liu et al, 2001;Lu et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

A Randomized Study of Biomimetic Peptides Efficacy and Impact on the Growth Factors Expression in the Hair Follicles of Patients with Telogen Effluvium

2018

J App Pharma Sci

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Currently, biomimetic peptides have been developed to treat alopecia, which consists of amino acid residues and are able to selectively interact with cell receptors. This article studies the expression of growth factors (VEGF, KGF, EGF, TGF-β1) in the hair follicle of patients with telogen effluvium and healthy individuals and evaluating the efficacy of therapy with biomimetic peptides in patients with telogen effluvium based on clinical data and the dynamics. The method of immunofluorescence study of scalp specimens, which is taken by the punch biopsy from the frontotemporal areas before and after the therapy, was used. 30 female patients with telogen effluvium aged between 20 and 56 years old were recruited for the research and randomly divided into two groups. Patients of group I were treated with lotion based on biomimetic peptides and those of group II were treated with 0.9% saline. The therapeutic efficacy of biomimetic peptides in women with telogen effluvium was assessed by trichoscopy and phototrichography. A change in the expression of VEGF, KGF, TGF-β1 growth factors was found in women with telogen effluvium as opposed to the healthy ones. After the therapy, a significant increase in the VEGF, EGF expression and a decrease in KGF and TGF-β1 expression were noted. The study proved the effectiveness of the proposed method of therapy for women with telogenic effluvium. The research findings can be useful to dermatologists and cosmetologists for increasing the effectiveness of therapy for patients with telogenic effluvium. Also, the data obtained in the article open up the prospect for the further study of the pathogenetic mechanisms of telogenic effluvium and provide an opportunity for an innovative approach to the therapy of patients with telogenic effluvium.

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“…These results suggested that β-catenin-dependent signalling also contributed to stabilization of the canonical TGF-β response. Activation of the canonical WNT signalling in response to TGF-β and the functional contribution of this mechanism to fibrotic processes have been observed not only during cardiac fibrogenesis, but also in other organs, including skin (Akhmetshina et al, 2012), lungs (Xu et al, 2017) and the hair follicles (Lu et al, 2016;Si et al, 2017, Plikus et al, 2012. Summarising, these data pointed to the important role of β-catenin-dependent pathway in TGF-β response.…”

Section: Regulation Of Canonical Wnt By Tgf-βmentioning

confidence: 99%

Crosstalk between TGF-β and WNT signalling pathways during cardiac fibrogenesis

2018

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Cardiac fibrosis is referred to as an excessive accumulation of stromal cells and extracellular matrix proteins in the myocardium. Progressive fibrosis causes stiffening of the cardiac tissue and affects conduction of electrical impulses, leading to heart failures in a broad range of cardiac conditions. At the cellular level, activation of the cardiac stromal cells and myofibroblast formation are considered as hallmarks of fibrogenesis. At the molecular level, transforming growth factor β (TGF-β) is traditionally considered as a master regulator of the profibrotic processes. More recently, the WNT signalling pathway has also been found to be implicated in the development of myocardial fibrosis. In this review, we summarize current knowledge on the involvement of TGF-β and WNT downstream molecular pathways to cardiac fibrogenesis and describe a crosstalk between these two profibrotic pathways. TGF-β and WNT ligands bind to different receptors and trigger various outputs. However, a growing body of evidence points to cross-regulation between these two pathways. It has been recognized that in cardiac pathologies TGF-β activates WNT/β-catenin signalling, which in turn stabilizes the TGF-β/Smad response. Furthermore both, the non-canonical TGF-β and non-canonical WNT signalling pathways, activate the same mitogen-activated protein kinases (MAPKs): the extracellular signal-regulated kinase (Erk), the c-Jun N-terminal kinases (JNKs) and p38. The crosstalk between TGF-β and WNT pathways seems to play an essential role in switching on the genetic machinery initiating profibrotic changes in the heart. Better understanding of these mechanisms will open new opportunities for development of targeted therapeutic approaches against cardiac fibrosis in the future.

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An investigation of crosstalk between Wnt/β-catenin and transforming growth factor-β signaling in androgenetic alopecia

Cited by 38 publications

References 22 publications

Finasteride Enhances Stem Cell Signals of Human Dermal Papilla Cells

Finasteride Enhances Stem Cell Signals of Human Dermal Papilla Cells

A Randomized Study of Biomimetic Peptides Efficacy and Impact on the Growth Factors Expression in the Hair Follicles of Patients with Telogen Effluvium

Crosstalk between TGF-β and WNT signalling pathways during cardiac fibrogenesis

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