Notch1 Signaling Regulates Wound Healing via Changing the Characteristics of Epidermal Stem Cells

Shu, Bin; Yang, Rui

doi:10.4172/2157-7633.1000348

Cited by 7 publications

(7 citation statements)

References 31 publications

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“…Notch1 and its ligand Jagged1 are up-regulated at the wound edge in grafted human skin on the nude mouse 16 . Consistent to our findings, Notch1 is up-regulated in the epidermis including suprabasal and basal laminal keratinocytes at 1~4 days after wounding in the mouse skin 30 , 46 . Up-regulated Notch1 activates TNFα expression, which can induce CCL20 and CXCL13 chemokine expression, leading to the recruitment of RORγ + group3 innate lymphoid cells in wounded skin 30 .…”

Section: Discussionsupporting

confidence: 91%

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JMJD3 and NF-κB-dependent activation of Notch1 gene is required for keratinocyte migration during skin wound healing

Shin

Jeong

et al. 2017

Sci Rep

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It has been shown that epigenetic regulation plays an important role in skin wound healing. We previously found that histone H3K27me3 demethylase JMJD3 regulates inflammation and cell migration in keratinocyte wound healing. In this study, we identified Notch1 as a direct target of JMJD3 and NF-κB in wounded keratinocytes using in vitro cell and in vivo animal models. We found that Notch1 is up-regulated in the wound edge and its expression is dependent on JMJD3 and NF-κB in wounded keratinocytes. We also found that Notch1 activates the expression of RhoU and PLAU gene, which are critical regulators of cell migration. Consistently, depletion or inactivation of Notch1 resulted in decreased filopodia formation, increased focal adhesion and actin stress fiber, leading to reduced keratinocyte migration and skin wound healing. Thus, our findings provide the molecular mechanism involving JMJD3/NF-κB-Notch pathway in keratinocyte wound healing.

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Section: Discussionsupporting

confidence: 91%

“…The inhibition of Notch by antisense RNA or γ-secretase inhibitor DAPT showed impaired skin wound healing due to inhibition of leukocyte infiltration, angiogenesis, and keratinocyte migration 47 , 48 . DAPT-treated wound also showed incomplete wound closure 46 , 49 .…”

Section: Discussionmentioning

confidence: 99%

JMJD3 and NF-κB-dependent activation of Notch1 gene is required for keratinocyte migration during skin wound healing

Shin

Jeong

et al. 2017

Sci Rep

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“…Previous study has shown that scar tissue exhibits lower number of ESCs and higher number of MFB than normal skin [10]. More recently, we demonstrated that this phenomenon is dependent on the activation of Notch/Jagged1 signaling pathway [11,12]. Activation of the Notch1/ Jagged1 pathway can promote ESC proliferation and inhibit the cells' differentiation to MFB [13,14].…”

Section: Introductionmentioning

confidence: 71%

microRNA-203 Modulates Wound Healing and Scar Formation via Suppressing Hes1 Expression in Epidermal Stem Cells

Zhou

Shu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Little is known how miR-203 is involved in epidermal stem cells (ESCs) differentiation and scar formation. Methods: We first used luciferase assay to determine the interaction of miR-203 with the 3’-UTR in regulation of Hes1 expression. We then used flow cytometry to analyze the effects of miR-203 expression on the differentiation of ESCs to MFB by determination of CK15 ratio and α-SMA. To confirm the results of flow cytometry analysis, we used Western blot to examine the expression of α-SMA, Collagen I (Col I), and Collagen III (Col III), as well as the expression of Notch1, Jagged1, and Hes1 in ESCs after the treatment of pre-miR-203 or anti-miR-203. Finally, we examined the effects local anti-miR-203 treatment on would closure and scar formation using a mouse skin wound model. Results: Pre-miR-203 treatment increased ESCs differentiation to MFB cells, as indicated by decreased CK15 ratio and increased MFB biomarkers. This phenomenon was reversed by overexpression of Hes1 in ESCs. In addition, skin incision increased expression of miR-203 in wound tissue. Local treatment of anti-miR-203 could accelerate wound closure and reduce scar formation in vivo, which was associated with increased re-epithelialization, skin attachment regeneration, and collagen reassignment. Finally, we confirmed that anti-miR-203 treatment could inhibit ESCs differentiation in vivo via increasing Hesl expression. Conclusion: Taken together, our results suggested that overexpression of miR-203 in ESCs after skin wound may be a critical mechanism underlying the scar formation.

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“…In our study, both of STX7 and PLLP were significantly downregulated in diabetic patient skin. The Notch1 pathway is a key regulator of wound healing [102]. Thus, defects in this pathway may be potential targets for improving healing in diabetes.…”

Section: Cytoskeleton Membrane and Adhesion Related Genesmentioning

confidence: 99%

Genome wide analysis of gene expression changes in skin from patients with type 2 diabetes

et al. 2020

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Notch1 Signaling Regulates Wound Healing via Changing the Characteristics of Epidermal Stem Cells

Cited by 7 publications

References 31 publications

JMJD3 and NF-κB-dependent activation of Notch1 gene is required for keratinocyte migration during skin wound healing

JMJD3 and NF-κB-dependent activation of Notch1 gene is required for keratinocyte migration during skin wound healing

microRNA-203 Modulates Wound Healing and Scar Formation via Suppressing Hes1 Expression in Epidermal Stem Cells

Genome wide analysis of gene expression changes in skin from patients with type 2 diabetes

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