scholarly journals IFI27, a novel epidermal growth factor-stabilized protein, is functionally involved in proliferation and cell cycling of human epidermal keratinocytes

2015 ◽  
Vol 48 (2) ◽  
pp. 187-197 ◽  
Author(s):  
W.-L. Hsieh ◽  
Y.-H. Huang ◽  
T.-M. Wang ◽  
Y.-C. Ming ◽  
C.-N. Tsai ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
Epidermal Growth ◽  
Cell Cycling

scholarly journals Parallel responses of human epidermal keratinocytes to inorganic SbIII and AsIII

2016 ◽  
Vol 13 (6) ◽  
pp. 963 ◽  
Author(s):  
Marjorie A. Phillips ◽  
Angela Cánovas ◽  
Pei-Wen Wu ◽  
Alma Islas-Trejo ◽  
Juan F. Medrano ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Target Cell ◽  
Biological Systems ◽  
Protein Profiling ◽  
Epidermal Keratinocytes ◽  
Proliferative Potential ◽  
Cell Type ◽  
Human Epidermal Keratinocytes ◽  
Epidermal Growth

Environmental contextIncreasing commercial use of antimony is raising its environmental presence and thus possible effects on humans and ecosystems. An important uncertainty is the risk that exposure poses for biological systems. The present work explores the similarity in response of human epidermal keratinocytes, a known target cell type, to antimony and arsenic, where deleterious consequences of exposure to the latter are better known. AbstractSbIII and AsIII are known to exhibit similar chemical properties, but the degree of similarity in their effects on biological systems merits further exploration. The present work compares the responses of human epidermal keratinocytes, a known target cell type for arsenite-induced carcinogenicity, to these metalloids after treatment for 1 week at environmentally relevant concentrations. Previous work with these cells has shown that arsenite and antimonite have parallel effects in suppressing differentiation, altering levels of several critical enzymes and maintaining colony-forming ability. More globally, protein profiling now reveals parallels in SbIII and AsIII effects. The more sensitive technique of transcriptional profiling also shows considerable parallels. Thus, gene expression changes were almost entirely in the same directions for the two treatments, although the degree of change was sometimes significantly different. Inspection of the changes revealed that RYR1 and LRIG1 were among the genes strongly suppressed, consistent with reduced calcium-dependent differentiation and maintenance of epidermal growth factor-dependent proliferative potential. Moreover, levels of microRNAs in the cells were altered in parallel, with nearly 90% of the 198 most highly expressed ones being suppressed. Among these was miR-203, which is known to decrease proliferative potential. Finally, both SbIII and AsIII were seen to attenuate bone morphogenetic protein 6 induction of dual-specificity phosphatases 2 and 14, consistent with maintaining epidermal growth factor receptor signalling. These findings raise the question of whether SbIII, like AsIII, could act as a human skin carcinogen.

scholarly journals Epidermal Growth Factor Relieves Inflammatory Signals inStaphylococcus aureus-Treated Human Epidermal Keratinocytes and Atopic Dermatitis-Like Skin Lesions in Nc/Nga Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Sun Young Choi ◽  
You Jin Lee ◽  
Ji Min Kim ◽  
Hyun Ji Kang ◽  
Sang Hyun Cho ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Opposite Effect ◽  
Egf Receptor ◽  
Skin Lesions ◽  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
Epidermal Growth

Atopic dermatitis (AD) is a chronic inflammatory skin disease with a defective immunologic barrier, which is aggravated byStaphylococcus aureus (S. aureus). Epidermal growth factor (EGF) suppresses inflammation and EGF receptor inhibitors increasedS. aureuscolonization. Thus, we investigated the potential roles of EGF in AD, which is often aggravated byS. aureus. We determined how EGF affects the expression of inflammatory cytokines and antimicrobial peptides (AMPs) in human epidermal keratinocytes (HEKs) treated with heat-inactivatedS. aureus(HKSA)in vitroand 2,4-dinitrochlorobenzene-induced AD-like skin lesions in Nc/Nga mice. HKSA increased IL-6 and NFκB expression; EGF treatment had the opposite effect. EGF increased humanβdefensin-2 expression in HEKs and murineβdefensin-3 in mice. In mice, both EGF and pimecrolimus groups showed less erythema with significantly reduced inflammation and decreased expression of thymic stromal lymphopoietin. EGF relievedS. aureus-induced inflammation and AD-like skin lesions in Nc/Nga mice. Therefore, EGF could be a potential topical treatment for AD.

Corrigendum to: Parallel responses of human epidermal keratinocytes to inorganic SbIII and AsIII

2019 ◽  
Vol 16 (1) ◽  
pp. 80
Author(s):  
Marjorie A. Phillips ◽  
Angela Cánovas ◽  
Pei-Wen Wu ◽  
Alma Islas-Trejo ◽  
Juan F. Medrano ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Target Cell ◽  
Biological Systems ◽  
Protein Profiling ◽  
Epidermal Keratinocytes ◽  
Proliferative Potential ◽  
Cell Type ◽  
Human Epidermal Keratinocytes ◽  
Epidermal Growth

Environmental contextIncreasing commercial use of antimony is raising its environmental presence and thus possible effects on humans and ecosystems. An important uncertainty is the risk that exposure poses for biological systems. The present work explores the similarity in response of human epidermal keratinocytes, a known target cell type, to antimony and arsenic, where deleterious consequences of exposure to the latter are better known. AbstractSbIII and AsIII are known to exhibit similar chemical properties, but the degree of similarity in their effects on biological systems merits further exploration. The present work compares the responses of human epidermal keratinocytes, a known target cell type for arsenite-induced carcinogenicity, to these metalloids after treatment for 1 week at environmentally relevant concentrations. Previous work with these cells has shown that arsenite and antimonite have parallel effects in suppressing differentiation, altering levels of several critical enzymes and maintaining colony-forming ability. More globally, protein profiling now reveals parallels in SbIII and AsIII effects. The more sensitive technique of transcriptional profiling also shows considerable parallels. Thus, gene expression changes were almost entirely in the same directions for the two treatments, although the degree of change was sometimes significantly different. Inspection of the changes revealed that RYR1 and LRIG1 were among the genes strongly suppressed, consistent with reduced calcium-dependent differentiation and maintenance of epidermal growth factor-dependent proliferative potential. Moreover, levels of microRNAs in the cells were altered in parallel, with nearly 90% of the 198 most highly expressed ones being suppressed. Among these was miR-203, which is known to decrease proliferative potential. Finally, both SbIII and AsIII were seen to attenuate bone morphogenetic protein 6 induction of dual-specificity phosphatases 2 and 14, consistent with maintaining epidermal growth factor receptor signalling. These findings raise the question of whether SbIII, like AsIII, could act as a human skin carcinogen.

Members of the src and ras oncogene families supplant the epidermal growth factor requirement of BALB/MK-2 keratinocytes and induce distinct alterations in their terminal differentiation program

1985 ◽  
Vol 5 (12) ◽  
pp. 3386-3396
Author(s):  
B Weissman ◽  
S A Aaronson
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Terminal Differentiation ◽  
Epidermal Keratinocytes ◽  
Ras Oncogene ◽  
Rapid Loss ◽  
Naturally Occurring ◽  
Epidermal Growth ◽  
Transforming Genes ◽  
Mouse Epidermal Keratinocytes

BALB-/MK-2 mouse epidermal keratinocytes required epidermal growth factor for proliferation and terminally differentiated in response to high Ca2+ concentration. Infection with retroviruses containing transforming genes of the src and ras oncogene families led to rapid loss of epidermal growth factor dependence, in some cases, accompanied by alterations in cellular morphology. The virus-altered cells continued to proliferate in the presence of high levels of extracellular calcium but exhibited alterations in normal keratinocyte terminal differentiation that appear to be specific to the particular oncogene. These alterations bore similarities to abnormalities in differentiation observed in naturally occurring squamous epithelial malignancies.

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