scholarly journals Caffeine Promotes Ultraviolet B-induced Apoptosis in Human Keratinocytes without Complete DNA Repair

2011 ◽  
Vol 286 (26) ◽  
pp. 22825-22832 ◽  
Author(s):  
Weinong Han ◽  
Mei Ming ◽  
Yu-Ying He
Keyword(s):  
Dna Repair ◽  
Human Keratinocytes ◽  
Ultraviolet B ◽  
Induced Apoptosis

scholarly journals UVB protective effects of Sargassum horneri through the regulation of Nrf2 mediated antioxidant mechanism

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Eui Jeong Han ◽  
Seo-Young Kim ◽  
Hee-Jin Han ◽  
Hyun-Soo Kim ◽  
Kil-Nam Kim ◽  
...  
Keyword(s):  
Skin Barrier ◽  
Human Keratinocytes ◽  
Underlying Mechanism ◽  
Ultraviolet B ◽  
Sargassum Horneri ◽  
Cellular Damage ◽  
Protective Effects ◽  
Skin Damage ◽  
Antioxidant Mechanism ◽  
Induced Apoptosis

AbstractThe present study aimed to evaluate the protective effect of a methanol extract of Sargassum horneri (SHM), which contains 6-hydroxy-4,4,7a-trimethyl-5,6,7,7a-tetrahydrobenzofuran-2(4H)-one (HTT) and apo-9′-fucoxanthinone, against ultraviolet B (UVB)-induced cellular damage in human keratinocytes and its underlying mechanism. SHM significantly improved cell viability of UVB-exposed human keratinocytes by reducing the generation of intracellular reactive oxygen species (ROS). Moreover, SHM inhibited UVB exposure-induced apoptosis by reducing the formation of apoptotic bodies and the populations of the sub-G1 hypodiploid cells and the early apoptotic cells by modulating the expression of the anti- and pro-apoptotic molecules, Bcl-2 and Bax, respectively. Furthermore, SHM inhibited NF-κB p65 activation by inducing the activation of Nrf2/HO-1 signaling. The cytoprotective and antiapoptotic activities of SHM are abolished by the inhibition of HO-1 signaling. In further study, SHM restored the skin dryness and skin barrier disruption in UVB-exposed human keratinocytes. Based to these results, our study suggests that SHM protects the cells against UVB-induced cellular damages through the Nrf2/HO-1/NF-κB p65 signaling pathway and may be potentially useful for the prevention of UVB-induced skin damage.

A novel apoptosis inducer, apoptosis signal regulating kinase (ASK1), is involved in ultraviolet B-induced apoptosis of cultured human keratinocytes

1998 ◽  
Vol 16 ◽  
pp. S69 ◽  
Author(s):  
Koji Sayama ◽  
Hidenori Ichijo ◽  
Kenshi Yamasaki ◽  
Yashushi Hanakawa ◽  
Yuji Shirakata ◽  
...  
Keyword(s):  
Human Keratinocytes ◽  
Ultraviolet B ◽  
Apoptosis Inducer ◽  
Induced Apoptosis

scholarly journals Ultraviolet B radiation-induced apoptosis in human keratinocytes: cytosolic activation of procaspase-8 and the role of Bcl-2

FEBS Letters ◽  
2003 ◽  
Vol 540 (1-3) ◽  
pp. 125-132 ◽  
Author(s):  
Zerihun Assefa ◽  
Marjan Garmyn ◽  
Annelies Vantieghem ◽  
Wim Declercq ◽  
Peter Vandenabeele ◽  
...  
Keyword(s):  
Human Keratinocytes ◽  
Ultraviolet B ◽  
Ultraviolet B Radiation ◽  
Radiation Induced ◽  
Induced Apoptosis

Effect of Retinoic Acid on Apoptosis and DNA Repair in Human Keratinocytes after UVB Irradiation

2000 ◽  
Vol 4 (1) ◽  
pp. 2-7 ◽  
Author(s):  
Gang Li ◽  
Jason A. Bush ◽  
Vincent C. Ho
Keyword(s):  
Dna Repair ◽  
Retinoic Acid ◽  
Skin Cancer ◽  
Human Keratinocytes ◽  
Epidemiological Studies ◽  
Skin Carcinogenesis ◽  
Apoptosis Assay ◽  
Initiation Stage ◽  
Induced Apoptosis ◽  
Damaged Dna

Background: Skin cancer is extremely common. Epidemiological studies indicated that ultraviolet radiation (UV) is the primary cause for skin cancers, and that retinoic acid (RA) is able to inhibit this UV-induced skin carcinogenesis; however, the molecular mechanism of the anti-UV action of RA is unclear. Objective: The purpose of this study is to investigate if RA enhances the removal of UV-induced DNA damage. Methods: The effect of RA on UV-induced apoptosis and DNA repair was investigated by ELISA apoptosis assay and CAT assay. Results: Both all-trans-RA and 9-cis-RA did not promote UV-induced apoptosis nor the repair of UV-damaged DNA in human keratinocytes. Furthermore, RA did not induce the expression of p53. Conclusion: The inhibition of RA on skin carcinogenesis is not due to enhanced removal of UV-damaged DNA. Therefore, RA does not inhibit skin cancer development at the initiation stage, but possibly at the promotion and progression stages.

scholarly journals Paeoniflorin attenuates ultraviolet B-induced apoptosis in human keratinocytes by inhibiting the ROS-p38-p53 pathway

2016 ◽  
Vol 13 (4) ◽  
pp. 3553-3558 ◽  
Author(s):  
LINGWEN KONG ◽  
SHANGSHANG WANG ◽  
XIAO WU ◽  
FUGUO ZUO ◽  
HAIHONG QIN ◽  
...  
Keyword(s):  
Human Keratinocytes ◽  
Ultraviolet B ◽  
P53 Pathway ◽  
Induced Apoptosis

scholarly journals Hesperidin Attenuates Ultraviolet B-Induced Apoptosis by Mitigating Oxidative Stress in Human Keratinocytes

2016 ◽  
Vol 24 (3) ◽  
pp. 312-319 ◽  
Author(s):  
Susara Ruwan Kumara Madduma Hewage ◽  
Mei Jing Piao ◽  
Kyoung Ah Kang ◽  
Yea Seong Ryu ◽  
Xia Han ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Human Keratinocytes ◽  
Ultraviolet B ◽  
Induced Apoptosis

scholarly journals Translational control of a human CDKN1A mRNA splice variant regulates the fate of UVB-irradiated human keratinocytes

2018 ◽  
Vol 29 (1) ◽  
pp. 29-41 ◽  
Author(s):  
Ann E. Collier ◽  
Dan F. Spandau ◽  
Ronald C. Wek
Keyword(s):  
Dna Repair ◽  
Cell Fate ◽  
Translational Control ◽  
Splice Variant ◽  
Mrna Translation ◽  
Human Keratinocytes ◽  
Ultraviolet B ◽  
G1 Arrest ◽  
Adaptive Responses ◽  
Mrna Splice

In response to sublethal ultraviolet B (UVB) irradiation, human keratinocytes transiently block progression of the cell cycle to allow ample time for DNA repair and cell fate determination. These cellular activities are important for avoiding the initiation of carcinogenesis in skin. Central to these processes is the repression of initiation of mRNA translation through GCN2 phosphorylation of eIF2α (eIF2α-P). Concurrent with reduced global protein synthesis, eIF2α-P and the accompanying integrated stress response (ISR) selectively enhance translation of mRNAs involved in stress adaptation. In this study, we elucidated a mechanism for eIF2α-P cytoprotection in response to UVB in human keratinocytes. Loss of eIF2α-P induced by UVB diminished G1 arrest, DNA repair, and cellular senescence coincident with enhanced cell death in human keratinocytes. Genome-wide analysis of translation revealed that the mechanism for these critical adaptive responses by eIF2α-P involved induced expression of CDKN1A encoding the p21 (CIP1/WAF1) protein. We further show that human CDKN1A mRNA splice variant 4 is preferentially translated following stress-induced eIF2α-P by a mechanism mediated in part by upstream ORFs situated in the 5′-leader of CDKN1A mRNA. We conclude that eIF2α-P is cytoprotective in response to UVB by a mechanism featuring translation of a specific splice variant of CDKN1A that facilitates G1 arrest and subsequent DNA repair.

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