scholarly journals A p38MAPK/HIF-1 Pathway Initiated by UVB Irradiation Is Required to Induce Noxa and Apoptosis of Human Keratinocytes

2010 ◽  
Vol 130 (9) ◽  
pp. 2269-2276 ◽  
Author(s):  
Kris Nys ◽  
An Van Laethem ◽  
Carine Michiels ◽  
Noemi Rubio ◽  
Jacques G. Piette ◽  
...  
2021 ◽  
Vol 22 (18) ◽  
pp. 9956
Author(s):  
Piotr Wójcik ◽  
Agnieszka Gęgotek ◽  
Neven Žarković ◽  
Elżbieta Skrzydlewska

Although apoptosis of keratinocytes has been relatively well studied, there is a lack of information comparing potentially proapoptotic treatments for healthy and diseased skin cells. Psoriasis is a chronic autoimmune-mediated skin disease manifested by patches of hyperproliferative keratinocytes that do not undergo apoptosis. UVB phototherapy is commonly used to treat psoriasis, although this has undesirable side effects, and is often combined with anti-inflammatory compounds. The aim of this study was to analyze if cannabidiol (CBD), a phytocannabinoid that has anti-inflammatory and antioxidant properties, may modify the proapoptotic effects of UVB irradiation in vitro by influencing apoptotic signaling pathways in donor psoriatic and healthy human keratinocytes obtained from the skin of five volunteers in each group. While CBD alone did not have any major effects on keratinocytes, the UVB treatment activated the extrinsic apoptotic pathway, with enhanced caspase 8 expression in both healthy and psoriatic keratinocytes. However, endoplasmic reticulum (ER) stress, characterized by increased expression of caspase 2, was observed in psoriatic cells after UVB irradiation. Furthermore, decreased p-AKT expression combined with increased 15-d-PGJ2 level and p-p38 expression was observed in psoriatic keratinocytes, which may promote both apoptosis and necrosis. Application of CBD partially attenuated these effects of UVB irradiation both in healthy and psoriatic keratinocytes, reducing the levels of 15-d-PGJ2, p-p38 and caspase 8 while increasing Bcl2 expression. However, CBD increased p-AKT only in UVB-treated healthy cells. Therefore, the reduction of apoptotic signaling pathways by CBD, observed mainly in healthy keratinocytes, suggests the need for further research into the possible beneficial effects of CBD.


Marine Drugs ◽  
2017 ◽  
Vol 15 (9) ◽  
pp. 268 ◽  
Author(s):  
Mei Piao ◽  
Kyoung Kang ◽  
Yea Ryu ◽  
Kristina Shilnikova ◽  
Jeong Park ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Jung Hwan Oh ◽  
Jung Im Lee ◽  
Fatih Karadeniz ◽  
So Young Park ◽  
Youngwan Seo ◽  
...  

UVB exposure is one of the causes of several skin complications including but not limited to premature aging, wrinkle formation, and hyperpigmentation. UV-induced skin aging is called photoaging, and oxidative stress-induced overexpression of matrix metalloproteinases (MMPs) is the main reason behind the photoaging-mediated collagen degradation. Natural origin inhibitors of MMPs are regarded as a promising approach to prevent or treat photoaging. Therefore, the present study investigated the protective effects of 3,5-dicaffeoyl-epi-quinic acid (DCEQA) in human HaCaT keratinocytes against UVB irradiation-related dysregulation of MMPs. Changes in the mRNA and protein expression and release of MMP-1, -2, and -9 were observed after UVB irradiation with or without DCEQA treatment. In addition, the effect of DCEQA on the activation of p38, JNK, and ERK MAPKs was analyzed. Treatment of UVB-irradiated HaCaT cells with 10 μM DCEQA significantly suppressed the overexpression of both mRNA and protein of MMP-1, -2, and -9 while slightly increasing the diminished type I procollagen production. UVB-induced activation of MAPKs was also ameliorated by DCEQA treatment in a dose-dependent manner. Results indicated that DCEQA treatment was able to protect keratinocytes from UVB-induced photoaging by inhibiting the stimulated production of MMPs and the related decrease in collagen production. It was suggested that DCEQA downregulated the collagen degradation via inhibition of MAPK activation, which resulted in decreased MMP activity.


Oncogene ◽  
2002 ◽  
Vol 21 (17) ◽  
pp. 2652-2661 ◽  
Author(s):  
Marjorie Chazal ◽  
Claire Marionnet ◽  
Laurence Michel ◽  
Karine Mollier ◽  
Jean-Eudes Dazard ◽  
...  

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e67632 ◽  
Author(s):  
Huey-Chun Huang ◽  
Tsong-Min Chang ◽  
Yu-Jia Chang ◽  
Hsin-Yun Wen

2008 ◽  
Vol 89 (9) ◽  
pp. 2303-2314 ◽  
Author(s):  
Linda Struijk ◽  
Els van der Meijden ◽  
Siamaque Kazem ◽  
Jan ter Schegget ◽  
Frank R. de Gruijl ◽  
...  

Epidemiological studies have shown an association between infections by specific betapapillomaviruses, such as human papillomavirus (HPV) types 5 and 8, and cutaneous squamous cell carcinoma (SCC). The role of betapapillomaviruses in the development of cutaneous SCC is, however, still enigmatic. The ability to inhibit UVB-induced apoptosis, as demonstrated for HPV5 in vitro, may be important in this respect, as survival of DNA-damaged and mutated cells increases the risk of transformation. The aim of this study was to assess whether inhibition of UVB-induced apoptosis is a general property of betapapillomaviruses and to identify apoptotic factors that are potentially involved in this process. Primary human keratinocytes transduced with E6 and E7 of selected betapapillomaviruses (HPV5, HPV8, HPV15, HPV20, HPV24 and HPV38) were characterized and subjected to UVB irradiation. HPV8- and HPV20-expressing keratinocytes in particular showed fewer signs of apoptosis, as demonstrated by lower levels of active caspase 3, less enzymic caspase activity and less DNA fragmentation. The observed inhibition of UVB-induced apoptosis was mediated by E6 and coincided with reduced steady-state expression of the pro-apoptotic protein Bax. In conclusion, E6 of HPV8 and HPV20 reduces the apoptotic responses upon UVB irradiation when expressed in primary human keratinocytes. Infections with HPV8 and HPV20 may therefore augment the carcinogenic effect of UV radiation and potentially contribute to oncogenic transformation of the skin.


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