Preclinical Radiobiology with Pions: RBE ? Values for Mouse Skin Damage as a Function of Single Doses of Pions

1979 ◽  
Vol 16 (3) ◽  
pp. 289-294 ◽  
Author(s):  
E. M. Fr�hlich ◽  
H. Blattmann ◽  
L. Pfister ◽  
I. Cordt ◽  
J. Zehnder ◽  
...  
Keyword(s):  
Mouse Skin ◽  
Skin Damage

scholarly journals Are FDA-Approved Sunscreen Components Effective in Preventing Solar UV-Induced Skin Cancer?

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1674
Author(s):  
Ann M. Bode ◽  
Eunmiri Roh
Keyword(s):  
Mouse Model ◽  
Mouse Skin ◽  
Hairless Mouse ◽  
Cutaneous Squamous Cell Carcinoma ◽  
Skin Carcinogenesis ◽  
Skin Damage ◽  
Solar Uv ◽  
Keratin 17 ◽  
Cox 2 ◽  
Solar Ultraviolet

Solar ultraviolet (SUV) exposure is a major risk factor in the etiology of cutaneous squamous cell carcinoma (cSCC). People commonly use sunscreens to prevent SUV-induced skin damage and cancer. Nonetheless, the prevalence of cSCC continues to increase every year, suggesting that commercially available sunscreens might not be used appropriately or are not completely effective. In the current study, a solar simulated light (SSL)-induced cSCC mouse model was used to investigate the efficacy of eight commonly used FDA-approved sunscreen components against skin carcinogenesis. First, we tested FDA-approved sunscreen components for their ability to block UVA or UVB irradiation by using VITRO-SKIN (a model that mimics human skin properties), and then the efficacy of FDA-approved sunscreen components was investigated in an SSL-induced cSCC mouse model. Our results identified which FDA-approved sunscreen components or combinations are effective in preventing cSCC development. Not surprisingly, the results indicated that sunscreen combinations that block both UVA and UVB significantly suppressed the formation of cutaneous papillomas and cSCC development and decreased the activation of oncoproteins and the expression of COX-2, keratin 17, and EGFR in SSL-exposed SKH-1 (Crl:SKH1-Hrhr) hairless mouse skin. Notably, several sunscreen components that were individually purported to block both UVA and UVB were ineffective alone. At least one component had toxic effects that led to a high mortality rate in mice exposed to SSL. Our findings provide new insights into the development of the best sunscreen to prevent chronic SUV-induced cSCC development.

scholarly journals Oenanthe Javanica Extract Protects Mouse Skin from UVB Radiation via Attenuating Collagen Disruption and Inflammation

2019 ◽  
Vol 20 (6) ◽  
pp. 1435 ◽  
Author(s):  
Young Her ◽  
Bich-Na Shin ◽  
Yun Lee ◽  
Joon Park ◽  
Dae Kim ◽  
...  
Keyword(s):  
Mouse Skin ◽  
Type Iii Collagen ◽  
Type I ◽  
Uvb Radiation ◽  
Skin Damage ◽  
Protein Levels ◽  
Photodamaged Skin ◽  
Tnf Α ◽  
Oenanthe Javanica ◽  
Cox 2

In recent years, the use of botanical agents to prevent skin damage from solar ultraviolet (UV) irradiation has received considerable attention. Oenanthe javanica is known to exert anti-inflammatory and antioxidant activities. This study investigated photoprotective properties of an Oenanthe javanica extract (OJE) against UVB-induced skin damage in ICR mice. The extent of skin damage was evaluated in three groups: control mice with no UVB, UVB-exposed mice treated with vehicle (saline), and UVB-exposed mice treated with 1% extract. Photoprotective properties were assessed in the dorsal skin using hematoxylin and eosin staining, Masson trichrome staining, immunohistochemical staining, quantitative real-time polymerase chain reaction, and western blotting to analyze the epidermal thickness, collagen expression, and mRNA and protein levels of type I collagen, type III collagen, and interstitial collagenases, including matrix metalloproteinase (MMP)-1 and MMP-3. In addition, tumor necrosis factor (TNF)-α and cyclooxygenase (COX)-2 protein levels were also assessed. In the UVB-exposed mice treated with extract, UV-induced epidermal damage was significantly ameliorated. In this group, productions of collagen types I and III were increased, and expressions of MMP-1 and MMP-3 were decreased. In addition, TNF-α and COX-2 expressions were reduced. Based on these findings, we conclude that OJE displays photoprotective effects against UVB-induced collagen disruption and inflammation and suggest that Oenanthe javanica can be used as a natural product for the treatment of photodamaged skin.

scholarly journals Targeting Angiogenesis by Blocking the ATM–SerRS–VEGFA Pathway for UV-Induced Skin Photodamage and Melanoma Growth

Cancers ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 1847 ◽  
Author(s):  
Yadong Song ◽  
Hongyan Lu ◽  
Qiong Wang ◽  
Rong Xiang
Keyword(s):  
Retinoic Acid ◽  
Cell Line ◽  
Uv Irradiation ◽  
Mouse Skin ◽  
Trna Synthetase ◽  
Angiogenic Factor ◽  
Skin Damage ◽  
Mouse Melanoma ◽  
Photo Damage

Retinoic acid (RA) has been widely used to protect skin from photo damage and skin carcinomas caused by solar ultraviolet (UV) irradiation, yet the mechanism remains elusive. Here, we report that all-trans retinoic acid (tRA) can directly induce the expression of a newly identified potent anti-angiogenic factor, seryl tRNA synthetase (SerRS), whose angiostatic role can, however, be inhibited by UV-activated ataxia telangiectasia mutated (ATM) kinase. In both a human epidermal cell line, HaCaT, and a mouse melanoma B16F10 cell line, we found that tRA could activate SerRS transcription through binding with the SerRS promoter. However, UV irradiation induced activation of ATM-phosphorylated SerRS, leading to the inactivation of SerRS as a transcriptional repressor of vascular endothelial growth factor A (VEGFA), which dampened the effect of tRA. When combined with ATM inhibitor KU-55933, tRA showed a greatly enhanced efficiency in inhibiting VEGFA expression and a much better protection of mouse skin from photo damage. Also, we found the combination greatly inhibited tumor angiogenesis and growth in mouse melanoma xenograft in vivo. Taken together, tRA combined with an ATM inhibitor can greatly enhance the anti-angiogenic activity of SerRS under UV irradiation and could be a better strategy in protecting skin from angiogenesis-associated skin damage and melanoma caused by UV radiation.

scholarly journals Therapeutic Effect of Seawater Pearl Powder on UV-Induced Photoaging in Mouse Skin

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Siyin Han ◽  
Delun Huang ◽  
Taijin Lan ◽  
Yongpei Wu ◽  
Yingbiao Wang ◽  
...  
Keyword(s):  
Therapeutic Effect ◽  
Mouse Skin ◽  
Mapk Signaling ◽  
Collagen I ◽  
Emission Spectrometry ◽  
Atomic Fluorescence Spectrometry ◽  
Histopathological Analysis ◽  
Skin Damage ◽  
Photoaged Skin ◽  
Matrix Metalloproteinase 1

The objective of this study was to investigate the therapeutic effect of seawater pearl powder (SPP) on ultraviolet (UV) irradiation-induced photoaging in mouse skin. The protein and trace elements in SPP were detected by liquid chromatography-mass spectrometry, atomic fluorescence spectrometry, and inductively coupled plasma-atomic emission spectrometry. The effect of SPP on treating skin damage resulting from UV-induced photoaging was observed by gross physical appearance and histopathological analysis. Oxidative stress and melanin synthesis were analyzed using biochemical method. Western blotting was applied to analyze the phosphorylation and expression levels of matrix metalloproteinase-1 (MMP-1), collagen I, and proteins involved in the mitogen-activated protein kinase (MAPK) signaling pathways (p38, ERK, and JNK). The results show that SPP has a significant therapeutic effect on UV-induced photoaging of skin and improves and restores appearance and tissue structure of mouse skin. The major mechanism may be related to reduction of expression level of MMP-1 and enhancement of collagen I production via inhibition of MAPK signaling pathway after scavenging of excess reactive oxygen species (ROS) in the UV-induced photoaged skin of mice. Meanwhile, it may also be involved in reducing melanin content by inhibiting tyrosinase activity after scavenging excess ROS in the UV-induced photoaged skin of mice. Therefore, SPP could be a good substance to treat photoaging skin. Taking cost-effectiveness and efficacy into consideration, the optimal concentration of SPP for treating photoaging skin could be 100 mg/g.

scholarly journals Role of distinct fibroblast lineages and immune cells in dermal repair following UV radiation induced tissue damage

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Emanuel Rognoni ◽  
Georgina Goss ◽  
Toru Hiratsuka ◽  
Kalle H Sipilä ◽  
Thomas Kirk ◽  
...  
Keyword(s):  
Dna Damage ◽  
Immune Cells ◽  
Mouse Skin ◽  
Cell Number ◽  
Lineage Tracing ◽  
Fibroblast Proliferation ◽  
Skin Damage ◽  
Solar Ultraviolet Radiation

Solar ultraviolet radiation (UVR) is a major source of skin damage, resulting in inflammation, premature ageing and cancer. While several UVR-induced changes, including extracellular matrix reorganisation and epidermal DNA damage, have been documented, the role of different fibroblast lineages and their communication with immune cells has not been explored. We show that acute and chronic UVR exposure led to selective loss of fibroblasts from the upper dermis in human and mouse skin. Lineage tracing and in vivo live imaging revealed that repair following acute UVR is predominantly mediated by papillary fibroblast proliferation and fibroblast reorganisation occurs with minimal migration. In contrast, chronic UVR exposure led to a permanent loss of papillary fibroblasts, with expansion of fibroblast membrane protrusions partially compensating for the reduction in cell number. Although UVR strongly activated Wnt-signalling in skin, stimulation of fibroblast proliferation by epidermal b-catenin stabilisation did not enhance papillary dermis repair. Acute UVR triggered an infiltrate of neutrophils and T cell subpopulations and increased pro-inflammatory prostaglandin signalling in skin. Depletion of CD4 and CD8 positive cells resulted in increased papillary fibroblast depletion, which correlated with an increase in DNA damage, pro-inflammatory prostaglandins and reduction in fibroblast proliferation. Conversely, topical COX-2 inhibition prevented fibroblast depletion and neutrophil infiltration after UVR. We conclude that loss of papillary fibroblasts is primarily induced by a deregulated inflammatory response, with infiltrating T cells supporting fibroblast survival upon UVR-induced environmental stress.

scholarly journals UV-Induced Keratin 1 Proteolysis Mediates UV-Induced Skin Damage

2017 ◽  
Author(s):  
Mingchao Zhang ◽  
Dhruba Tara Maharjan ◽  
Hao He ◽  
Yujia Li ◽  
Wei Yan ◽  
...  
Keyword(s):  
Cysteine Protease ◽  
Inflammatory Responses ◽  
Mouse Skin ◽  
Cysteine Protease Inhibitor ◽  
Skin Damage ◽  
Non Invasive ◽  
Prevention And Treatment ◽  
Uv Dose ◽  
Spinous Layer ◽  
Keratin 1

AbstractKeratins play critical roles in intermediate filament formation, inflammatory responses and cellular signaling in epithelium. While keratins is a major epidermal fluorophore, the mechanisms underlying the autofluorescence (AF) of keratins and its biomedical implications have remained unknown. Our study used mouse skin as a model to study these topics, showing that UV dose-dependently induced increases in green AF at the spinous layer of the epidermis of mouse within 6 hr of the UV exposures, which may be used for non-invasive prediction of UV-induced skin damage. The UV-induced AF appears to be induced by cysteine protease-mediated keratin 1 proteolysis: 1) UV rapidly induced significant keratin 1 degradation; 2) administration of keratin 1 siRNA largely decreased the UV-induced AF; and 3) administration of E-64, a cysteine protease inhibitor, significantly attenuated the UV-induced AF and keratin 1 degradation. Our study has also suggested that the UV-induced keratin 1 proteolysis may be a novel crucial pathological factor in UV-induced skin damage, which is supported by both the findings that indicate critical biological roles of keratin 1 in epithelium and our observation that prevention of UV-induced keratin 1 proteolysis can lead to decreased UV-induced skin damage. Collectively, our study has suggested that UV-induced keratin 1 proteolysis may be a novel and valuable target for diagnosis, prevention and treatment of UV-induced skin damage.

scholarly journals Role of distinct fibroblast lineages and immune cells in dermal repair following UV radiation induced tissue damage

2021 ◽  
Author(s):  
Emanuel Rognoni ◽  
Georgina Goss ◽  
Toru Hiratsuka ◽  
Katharina I Kober ◽  
Prudence PokWai Lui ◽  
...  
Keyword(s):  
Dna Damage ◽  
Immune Cells ◽  
Mouse Skin ◽  
Cell Number ◽  
Lineage Tracing ◽  
Fibroblast Proliferation ◽  
Skin Damage ◽  
Solar Ultraviolet Radiation

Solar ultraviolet radiation (UVR) is a major source of skin damage, resulting in inflammation, premature ageing and cancer. While several UVR-induced changes, including extracellular matrix reorganisation and epidermal DNA damage, have been documented, the role of different fibroblast lineages and their communication with immune cells has not been explored. We show that acute and chronic UVR exposure led to selective loss of fibroblasts from the upper dermis in human and mouse skin. Lineage tracing and in vivo live imaging revealed that repair following acute UVR is predominantly mediated by papillary fibroblast proliferation and migration. In contrast, chronic UVR exposure led to a permanent loss of papillary fibroblasts, with expansion of fibroblast membrane protrusions partially compensating for the reduction in cell number. Although UVR strongly activated Wnt-signalling in skin, stimulation of fibroblast proliferation by epidermal b-catenin stabilisation did not support papillary dermis repair. Acute UVR triggered an infiltrate of neutrophils and T cell subpopulations and increased pro-inflammatory prostaglandin signalling in skin. Depletion of CD4 and CD8 positive cells resulted in increased papillary fibroblast depletion, which correlated with an increase in DNA damage and reduction in fibroblast proliferation. Conversely, topical COX-2 inhibition prevented fibroblast depletion and neutrophil infiltration after UVR. We conclude that loss of papillary fibroblasts is primarily induced by a deregulated inflammatory response, with infiltrating T cells supporting fibroblast survival upon UVR-induced environmental stress.

scholarly journals Coenzyme Q10 Sunscreen Prevents Progression of Ultraviolet-Induced Skin Damage in Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Haiyou Wu ◽  
Zhangfeng Zhong ◽  
Sien Lin ◽  
Chuqun Qiu ◽  
Peitao Xie ◽  
...  
Keyword(s):  
Coenzyme Q ◽  
Rapid Development ◽  
Mouse Skin ◽  
Skin Surface ◽  
Positive Control ◽  
Ultraviolet B ◽  
Control Group ◽  
Skin Damage ◽  
Ultraviolet Ray ◽  
Underlying Mechanisms

The level of sun ultraviolet ray reaching the surface of the earth is increasing severely due to the rapid development of the society and environmental destruction. Excessive exposure to ultraviolet radiation causes skin damage and photoaging. Therefore, it is emerged to develop effective sunscreen to prevent ultraviolet-induced skin damage. This study was aimed at investigating the effects of Coenzyme Q10 (CoQ10) sunscreen on the prevention of ultraviolet B radiation- (UVB-) induced mouse skin damage. Three-month-old female mice were used, and they were randomly divided into four groups: control, model, CoQ10, and titanium dioxide (TiO2; positive control) groups. Our results showed that body weight, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, and DNA (cytosine-5)-methyltransferase 1 (DNMT1) protein expression were significantly decreased, while malondialdehyde (MDA) activity and metalloproteinase-1 (MMP-1) level were increased in UVB-treated mice. Besides, the stratum corneum was shed from the skin surface in the model group compared with the control group. In contrast, CoQ10 sunscreen prevented from UVB-induced skin damage, as well as reversing SOD, GSH-Px, and MDA activities, and MMP-1 and DNMT1 levels. Taken together, the current study provided further evidence on the prevention of UVB-induced skin damage by CoQ10 and its underlying mechanisms.

scholarly journals PM 10 Exposure Induced IL-1β and IL-6 Expression in Hairless Mouse Skin

2021 ◽  
Vol 27 (4) ◽  
pp. 898-902
Author(s):  
Min Kyung Kim ◽  
Jeong-hee Kim
Keyword(s):  
Western Blot ◽  
Skin Diseases ◽  
Mouse Skin ◽  
Hairless Mouse ◽  
Air Pollutant ◽  
Skin Damage ◽  
Inflammatory Skin Diseases ◽  
Expression Levels ◽  
Hairless Mouse Skin ◽  
Pm 10

More recently, air pollution is acknowledged as an immense risk factor for developing serious health issues, and particulate matter (PM10) are a common air pollutant. To evaluate the biological mechanisms of PM10 on skin damage. PM10 was applied to mouse skin at 10 µg/mL for 7 days. In this study, we analyzed that PM10-induced inflammation on hairless mouse skin by immunohistochemistry and western blot. As a result, immunohistochemical staining demonstrated that the IL-1β and IL-6 expression levels were increased after PM10 treatment. Moreover, the analysis of western blot suggested that PM10 treatment increased the expression levels of proinflammatory cytokines IL-1β (**<i>P</i><0.01) and IL-6 (**<i>P</i><0.05). In conclusion, our findings contribute to the understanding of the pathophysiological mechanisms of PM10 to the skin and can be used as a therapeutic strategy to control inflammatory skin diseases caused by PM10.

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