Retrotransposons have played an important role in evolution through their transposable activity. The largest and the only currently active human group of mobile DNAs are the retrotransposons. The ectopic expression of has been correlated with genomic instability. Narrow-band ultraviolet B (NB-UVB) and broad-band ultraviolet B (BB-UVB) phototherapy is commonly used for the treatment of dermatological diseases. UVB exposure is carcinogenic and can lead, in keratinocytes, to genomic instability. We hypothesize that reactivation occurs at a high rate in response to UVB exposure on the skin, which significantly contributes to genomic instability and DNA damage leading to cellular senescence and photoaging. Immortalized N/TERT1 and HaCaT human keratinocyte cell lines were irradiated in vitro with either NB-UVB or BB-UVB. Using immunofluorescence and Western blotting, we confirmed UVB-induced protein expression of LINE-1. Using RT-qPCR, we measured the mRNA expression of and senescence markers that were upregulated after several NB-UVB exposures. Selected miRNAs that are known to bind mRNA were measured using RT-qPCR, and the expression of was downregulated with UVB exposure. Our findings demonstrate that UVB irradiation induces reactivation and DNA damage in normal keratinocytes along with the associated upregulation of cellular senescence markers and change in expression.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10669206PMC
http://dx.doi.org/10.3390/biomedicines11113017DOI Listing

Publication Analysis

Top Keywords

cellular senescence
12
genomic instability
12
uvb exposure
12
ectopic expression
8
expression line-1
8
dna damage
8
senescence markers
8
expression
6
ultraviolet irradiation
4
irradiation keratinocytes
4

Similar Publications

Cellular senescence is a phenotypic state that contributes to the progression of age-related disease through secretion of pro-inflammatory factors known as the senescence-associated secretory phenotype (SASP). Understanding the process by which healthy cells become senescent and develop SASP factors is critical for improving the identification of senescent cells and, ultimately, understanding tissue dysfunction. Here, we reveal how the duration of cellular stress modulates the SASP in distinct subpopulations of senescent cells.

View Article and Find Full Text PDF

Background: The clinical course of high-risk neuroblastoma patients remains suboptimal, and the dynamic and reversible nature of cellular senescence provides an opportunity to develop new therapies.

Objective: This study aims to identify unique markers of cellular senescence in neuroblastoma and to explore their clinical significance.

Methods: The impact of multiple genetic regulatory mechanisms on cellular senescence-associated genes (CSAGs) was first assessed.

View Article and Find Full Text PDF

Cellular senescence is understood to be a biological process that is defined as irreversible growth arrest and was originally recognized as a tumor-suppressive mechanism that prevents further propagation of damaged cells. More recently, cellular senescence has been shown to have a dual role in prevention and tumor promotion. Senescent cells carry a senescence-associated secretory phenotype (SASP), which is altered by secretory factors including pro-inflammatory cytokines, chemokines, and other proteases, leading to the alteration of the tissue microenvironment.

View Article and Find Full Text PDF

AP2A1 modulates cell states between senescence and rejuvenation.

Cell Signal

January 2025

Division of Bioengineering, Graduate School of Engineering Science, University of Osaka, Japan; R(3) Institute for Newly-Emerging Science Design, University of Osaka, Japan; Global Center for Medical Engineering and Informatics, University of Osaka, Japan. Electronic address:

Aging proceeds with the accumulation of senescent cells in multiple organs. These cells exhibit increased size compared to young cells, which promotes further senescence and age-related diseases. Currently, the molecular mechanism behind the maintenance of such huge cell architecture undergoing senescence remains poorly understood.

View Article and Find Full Text PDF

Humans can be exposed to LCCPs through air and diet, leading to their accumulation in the body. Given the significance of understanding potential health risks, a thorough investigation into the detrimental health impacts of LCCPs is paramount. In this study, we conducted a series of experiments to investigate the effects of LCCPs on cardiomyocytes, employing techniques such as flow cytometry, western-blot, indirect immunofluorescence, and confocal microscopy.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!