scholarly journals Study of the protective effects of cosmetic ingredients on the skin barrier, based on the expression of barrier-related genes and cytokines

2021 ◽  
Author(s):  
Wenyu Ding ◽  
Linna Fan ◽  
Yan Tian ◽  
Congfen He
Keyword(s):  
Sodium Dodecyl ◽  
Skin Barrier ◽  
Vascular Endothelial ◽  
Hacat Cells ◽  
Protective Effects ◽  
Sensitive Skin ◽  
Complex Process ◽  
Cosmetic Ingredients ◽  
Proliferation And Differentiation ◽  
Endothelial Growth Factor

Abstract Background Sensitive skin is the result of a complex process that is closely linked to the damage of the skin barrier. There are no recognized methods for evaluating the efficacy of anti-allergy products. Methods In this study, a model of skin barrier damage was created by treating HaCaT cells with 60 μg/ml of sodium dodecyl sulfate for 48 h. The protective effects of nine cosmetic ingredients, including oat extract (S1), on the skin barrier were investigated based on the gene expression levels of aquaporin3 (AQP3), filaggrin (FLG), caspase-14 (CASP14), and human tissue kallikrein7 (KLK7), as well as those of various interleukins (IL) and vascular endothelial growth factor (VEGF). Results Among the nine ingredients, S1 had a good protective effect on the function of the skin barrier. It promoted the expression of AQP3, FLG, and CASP14, while inhibiting the expression of KLK7 in HaCaT cells, at a concentration of 0.06%. It also maintained IL-6, IL-8, and VEGF at appropriate levels while promoting the proliferation and differentiation of HaCaT cells. Conclusions The above indicators allow for the preliminary establishment of a method to evaluate the efficacy of the barrier protection ability of sensitive skin.

scholarly journals Aster glehniExtract Containing Caffeoylquinic Compounds Protects Human Keratinocytes through the TRPV4-PPARδ-AMPK Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-13
Author(s):  
Yong-Jik Lee ◽  
Yoo-Na Jang ◽  
Yoon-Mi Han ◽  
Hyun-Min Kim ◽  
Changbae Jin ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Sodium Dodecyl ◽  
Skin Barrier ◽  
Human Keratinocytes ◽  
Control Group ◽  
Hacat Cells ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Protein Levels ◽  
Ampk Pathway

Aster glehni(AG) has been used in cooking and as a medicine to treat various diseases for over hundreds of years in Korea. To speculate the protective effects of AG on skin barrier, we estimated the protein levels of biomarkers related to skin barrier protection in human keratinocytes, HaCaT cells treated with sodium dodecyl sulfate (SDS), or 2,4-dinitrochlorobenzene (DNCB). The protein levels for keratin, involucrin, defensin, tumor necrosis factor alpha (TNFα), peroxisome proliferator-activated receptor delta (PPARδ), 5′ adenosine monophosphate-activated protein kinase (AMPK), serine palmitoyltransferase long chain base subunit 2 (SPTLC2), and transient receptor potential cation channel subfamily V member 4 (TRPV4) were evaluated using western blotting or immunocytochemistry in HaCaT cells. AG extract increased the protein levels of PPARδ, phosphorylated AMPK, SPTLC2, keratin, involucrin, and defensin compared to the SDS or DNCB control group. However, TNFαexpression increased by SDS or DNCB was decreased with AG extract. The order of action of each regulatory biomarker in AG pathway was identified TRPV4→PPARδ→AMPK from antagonist and siRNA treatment studies. AG can ameliorate the injury of keratinocytes caused by SDS or DNCB through the sequential regulation of TRPV4→PPARδ→AMPK pathway.

scholarly journals Vascular endothelial growth factor production is induced by histone deacetylase 1 and suppressed by von Hippel-Lindau protein in HaCaT cells

2012 ◽  
Vol 35 (6) ◽  
pp. 340 ◽  
Author(s):  
Angélica Reynoso-Roldán ◽  
Maria L Roldán ◽  
Juan C Cancino-Diaz ◽  
Sandra Rodríguez-Martínez ◽  
Mario E Cancino-Diaz
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Hacat Cells ◽  
Vegf Expression ◽  
Transfected Cells ◽  
Von Hippel Lindau ◽  
Histone Deacetylase 1 ◽  
Endothelial Growth Factor ◽  
In Cells

Purpose: In hypoxic tumoral tissues, vascular endothelial growth factor (VEGF) expression is positively regulated by histone deacetylase 1 (HDAC1) and negatively regulated by the tumour suppressor protein von Hippel-Lindau (VHL) via transforming growth factor-alpha (HIF-1alpha). It has been reported that VEGF, HDAC1 and LL-37, but not VHL, are over-expressed in psoriatic skin. Although HIF-1alpha is constitutively expressed in normal keratinocytes, it is not known if HDAC1 and VHL can regulate VEGF production in these cells. Methods: The participation of HDAC1 and VHL in the regulation of VEGF expression in HDAC-, VHL- and LL-37-transfected HaCaT cells, and in HaCaT cells treated with HDAC1 inhibitors, was studied. Results: The production of VEGF was increased in HDAC1- and LL-37-transfected HaCaT cells and maintained in VHL-transfected cells under hypoxic conditions; meanwhile, VEGF production decreased in HaCaT cells treated with TSA, in cells transfected with HDAC1-siRNA, in cells co-transfected with HIF-1alpha-siRNA and pHDAC-1 and in VHL-transfected HaCaT cells. The levels of cytoplasmic HIF-1alpha were high in pLL37-transfected cells and low in pVHL- and pHDAC1-transfected cells; however, HIF-1alpha was detected in the nucleus of the HDAC1-transfected cells. The expression of VEGF was high in cells co-transfected with pHDAC1- and pLL-37, and the expression decreased when pVHL was present. Conclusions: These data demonstrate that HDAC1, LL-37 and VHL can modulate the production of VEGF via HIF-1alpha in HaCaT cells.

scholarly journals Id2 Mediates Tumor Initiation, Proliferation, and Angiogenesis in Rb Mutant Mice

2005 ◽  
Vol 25 (9) ◽  
pp. 3563-3574 ◽  
Author(s):  
Anna Lasorella ◽  
Gerson Rothschild ◽  
Yoshifumi Yokota ◽  
Robert G. Russell ◽  
Antonio Iavarone
Keyword(s):  
Critical Role ◽  
Pituitary Tumors ◽  
Pituitary Cells ◽  
Vascular Endothelial ◽  
Tumor Initiation ◽  
Human Neuroblastoma ◽  
Helix Loop Helix ◽  
Proliferation And Differentiation ◽  
Early Tumor ◽  
Endothelial Growth Factor

ABSTRACT The inhibitor of differentiation Id2 is a target of the retinoblastoma (Rb) protein during mouse embryogenesis. In Rb +/− mice, LOH at the wild-type Rb allele initiates pituitary adenocarcinoma, a tumor derived from embryonic melanotropes. Here we identify a critical role for Id2 in initiation, growth, and angiogenesis of pituitary tumors from Rb +/− mice. We show that proliferation and differentiation are intimately coupled in Rb +/− pituitary cells before tumor initiation. In Id2-null pituitaries, premature activation of basic helix-loop-helix-mediated transcription and expression of the cdk inhibitor p27Kip1 impairs the proliferation of melanotropes and tumor initiation. Without Id2, Rb +/− mice have fewer early tumor lesions and a markedly decreased proliferation rate of the tumor foci. Expression of Id2 by pituitary tumor cells promotes growth and angiogenesis by functioning as a master regulator of vascular endothelial growth factor (VEGF). In human neuroblastoma, the N-Myc-driven expression of Id2 is sufficient and necessary for expression of VEGF. These results establish that aberrant Id2 activity directs initiation and progression of embryonal cancer.

scholarly journals Targeting Angiogenesis in Cancer Treatments: Where do we Stand?

2016 ◽  
Vol 19 (2) ◽  
pp. 226 ◽  
Author(s):  
Nenad Petrovic
Keyword(s):  
Cancer Progression ◽  
Angiogenesis Inhibitors ◽  
Tissue Growth ◽  
Vascular Endothelial ◽  
Cancer Treatments ◽  
Slowing Down ◽  
Complex Process ◽  
Simultaneous Inhibition ◽  
Endothelial Growth Factor ◽  
Multiple Signaling

Since early seventies of the twentieth century, through seminal work of Judah Folkman, angiogenesis, the process of new blood vessel sprouting from the existing vasculature, was recognized as a necessary part of wound healing, development of placenta, tissue growth and regeneration as well as cancer progression. This process is induced by low tissue oxygenation and it is a crucial prerequisite for rapid tissue growth, providing proper oxygen supply and removal of toxic metabolites. Suppression of angiogenesis as a way of slowing down tumor progression continues to be one of the most important areas of cancer research. The angiogenic process is relatively complex and it is regulated by numerous pro- and anti-angiogenic factors. Intensive research in the last twenty years resulted in identification of more than 300 angiogenesis inhibitors, a trend that is expected to continue. Unfortunately, most of these treatments have demonstrated unacceptable toxicities or failed to show activity in clinical studies. Although not yet completely understood, the complex process of tumor angiogenesis involves highly regulated orchestration of multiple activating and inhibiting factors. Vascular endothelial growth factor (VEGF) and its cognate receptors appear to play a central role in angiogenesis activation. Thus, initial efforts to develop anti-angiogenic treatments focused largely on inhibiting VEGF action. Such approaches, however, often lead to transient responses due to multiple pathways able to compensate for a single pathway inhibited. Accordingly, more recent treatments have focused on simultaneous inhibition of multiple signaling pathways. This review concentrates on identifying those anti-angiogenic treatments that made to the clinic by receiving approval by USA Food and Drug Administration (FDA) as treatments for cancer. Regardless of observed problems, it is an imperative that research in angiogenesis regulation continues. Consequently, pharmacological manipulation of angiogenesis may yet to introduce truly new pharmacological therapies into the field of cancer therapy, the field that was rather dormant in the last several decades. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

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