scholarly journals Epiprofin orchestrates epidermal keratinocyte proliferation and differentiation

2014 ◽  
Vol 127 (24) ◽  
pp. 5261-5272 ◽  
Author(s):  
T. Nakamura ◽  
Y. Yoshitomi ◽  
K. Sakai ◽  
V. Patel ◽  
S. Fukumoto ◽  
...  
Keyword(s):  
Keratinocyte Proliferation ◽  
Epidermal Keratinocyte ◽  
Proliferation And Differentiation

scholarly journals Hyaluronan Does Not Regulate Human Epidermal Keratinocyte Proliferation and Differentiation

2015 ◽  
Vol 291 (12) ◽  
pp. 6347-6358 ◽  
Author(s):  
Jérémy Malaisse ◽  
Valérie Pendaries ◽  
Fanny Hontoir ◽  
Valérie De Glas ◽  
Daniel Van Vlaender ◽  
...  
Keyword(s):  
Keratinocyte Proliferation ◽  
Epidermal Keratinocyte ◽  
Proliferation And Differentiation ◽  
Human Epidermal Keratinocyte

scholarly journals Role for WNT16B in human epidermal keratinocyte proliferation and differentiation

2007 ◽  
Vol 120 (5) ◽  
pp. 917-917 ◽  
Author(s):  
M.-T. Teh ◽  
D. Blaydon ◽  
L. R. Ghali ◽  
V. Briggs ◽  
S. Edmunds ◽  
...  
Keyword(s):  
Keratinocyte Proliferation ◽  
Epidermal Keratinocyte ◽  
Proliferation And Differentiation ◽  
Human Epidermal Keratinocyte

scholarly journals A Potential Role for Ceramide in the Regulation of Mouse Epidermal Keratinocyte Proliferation and Differentiation

1998 ◽  
Vol 110 (4) ◽  
pp. 318-323 ◽  
Author(s):  
EunMi Jung ◽  
Richard D. Griner ◽  
RaShawn Mann-Blakeney ◽  
Wendy Bollinger Bollag
Keyword(s):  
Potential Role ◽  
Keratinocyte Proliferation ◽  
Epidermal Keratinocyte ◽  
Proliferation And Differentiation

scholarly journals Role for WNT16B in human epidermal keratinocyte proliferation and differentiation

2007 ◽  
Vol 120 (2) ◽  
pp. 330-339 ◽  
Author(s):  
M.-T. Teh ◽  
D. Blaydon ◽  
L. R. Ghali ◽  
S. Edmunds ◽  
E. Pantazi ◽  
...  
Keyword(s):  
Keratinocyte Proliferation ◽  
Epidermal Keratinocyte ◽  
Proliferation And Differentiation ◽  
Human Epidermal Keratinocyte

scholarly journals The endoribonuclease N4BP1 prevents psoriasis by controlling both keratinocytes proliferation and neutrophil infiltration

2021 ◽  
Vol 12 (5) ◽  
Author(s):  
Chenliang Gou ◽  
Wenkai Ni ◽  
Panpan Ma ◽  
Fengbo Zhao ◽  
Zhou Wang ◽  
...  
Keyword(s):  
Physiological Role ◽  
Neutrophil Infiltration ◽  
Proper Function ◽  
Psoriatic Skin ◽  
Epidermal Keratinocytes ◽  
Keratinocyte Proliferation ◽  
Proliferation And Differentiation ◽  
Long Time ◽  
Chronic Skin ◽  
Upregulated Genes

AbstractPsoriasis is a common chronic skin disease, characterized by abnormal interplay between hyperproliferative epidermal keratinocytes and self-reactive immune cells with not fully addressed molecular mechanism. N4BP1 (NEDD4-binding protein 1) is considered as an immune regulator for a long time but its physiological role is not determined yet. Here, we found that the expression of N4BP1 in skin was highest among all 54 tested tissues, and its expression was further upregulated in psoriatic skin. N4BP1-deficient mice exhibited normal grossly, but developed severe and prolonged IMQ-induced psoriasis-like disease comparing to controls. N4BP1 mainly expressed in keratinocytes and located on nucleus. Up- but not downregulated genes in N4BP1-deficient skin were specifically enriched in keratinocyte proliferation and differentiation. The proliferation of N4BP1-deficient primary keratinocytes was faster compared to that of controls. The upregulated genes upon ablation of N4BP1 were highly enriched in targets of AP-1 transcription factor. Knocking out N4BP1 resulted in upregulation of JunB and FosB, and conversely, overexpression of N4BP1 greatly reduced their expression. Furthermore, N4BP1 binds with JunB and FosB encoding mRNAs and greatly reduces their stability. In addition, with a high expression in neutrophils, N4BP1 limits survival of neutrophils in blood and infiltration of neutrophils in psoriatic skin by targeting CXCL1, CCL20, and S100A8. These findings demonstrate that N4BP1 controls the proper function of keratinocytes and neutrophils by negatively regulating JunB, FosB, and CXCL1, respectively, and that is critical for psoriasis prevention.

Interleukin-6 promotes human epidermal keratinocyte proliferation and keratin cytoskeleton reorganization in culture

2006 ◽  
Vol 325 (1) ◽  
pp. 77-90 ◽  
Author(s):  
Miriam Hernández-Quintero ◽  
Walid Kuri-Harcuch ◽  
Arturo González Robles ◽  
Federico Castro-Muñozledo
Keyword(s):  
Interleukin 6 ◽  
Keratinocyte Proliferation ◽  
Epidermal Keratinocyte ◽  
Cytoskeleton Reorganization ◽  
Human Epidermal Keratinocyte

scholarly journals Mutant p63 affects epidermal cell identity through rewiring the enhancer landscape

2018 ◽  
Author(s):  
Jieqiong Qu ◽  
Sabine Tanis ◽  
Jos P.H. Smits ◽  
Evelyn N. Kouwenhoven ◽  
Martin Oti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Binding ◽  
Epidermal Cell ◽  
Developmental Disorders ◽  
Molecular Mechanisms ◽  
Epidermal Keratinocytes ◽  
Cell Identity ◽  
Keratinocyte Proliferation ◽  
Eec Syndrome ◽  
Proliferation And Differentiation

AbstractTranscription factor p63 is a key regulator of epidermal keratinocyte proliferation and differentiation. In humans mutations in p63 cause several developmental disorders with defects of ectoderm-derived structures including the epidermis. The underlying molecular mechanisms of these mutations however remain unclear. Here we characterized the transcriptome and epigenome from EEC syndrome patients carrying mutations in the p63 DNA-binding domain. The transcriptome of p63 mutant keratinocytes deviated from the normal epidermal cell identity. Epigenomic analyses showed that the deregulated gene expression in p63 mutant keratinocytes resulted from an altered enhancer landscape contributed by loss of p63-bound active enhancers and by unexpected gain of enhancers. The gained enhancers in mutant keratinocytes were frequently bound by deregulated transcription factors such as RUNX1. Reversing RUNX1 overexpression partially rescued deregulated gene expression as well as the enhancer distribution. Our findings support the pivotal role of p63 in controlling the enhancer landscape of epidermal keratinocytes and identify a novel mechanism whereby p63 DNA-binding mutations associated with EEC syndrome rewire the enhancer landscape and affect epidermal cell identity.

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