Notch 1 regulates keratinocyte migration via integrin beta1 activation during wound healing

Roy, Madhuchhanda; Jaraczewski, Taylor J.; Stofflet, John T.; Pathak, Priya; Schlosser, Sandy J.; Allen-Hoffmann, B. Lynn; T, King

doi:10.1016/j.jamcollsurg.2012.06.091

Cited by 1 publication

(1 citation statement)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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 . 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

View full text Add to dashboard Cite

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.

show abstract